AKG may increase Lifespan and DRAMATICALLY Increase Healthy Years

AKG may increase Lifespan and DRAMATICALLY Increase Healthy Years

Noting that some of the mice did experience moderate lifespan extension (the average was around 12%), measures of healthspan increased more than 40 percent. Lithgow says the goal is always to compress the time of disease and frailty. “The nightmare scenario has always been life extension with no reduction in disability. In this study, the treated middle-aged mice got healthier over time. Even the mice that died early saw improvements in their health, which was really surprising and encouraging.”

Citation: Alpha-ketoglutarate, an endogenous metabolite, extends lifespan and compresses morbidity in aging mice DOI: 10.1016/j.cmet 2020.08.044

https://www.sciencedirect.com/science/article/abs/pii/S1550413120304174#undfig1

Black raspberries show promise for reducing skin inflammation, allergies

Glutamine could help people with obesity reduce fat mass and inflammation

Glutamine could help people with obesity reduce fat mass and inflammation

Glutamine could help people with obesity reduce fat mass and inflammation

Lower glutamine-levels were also associated with larger fat cell size and higher body fat percentage independently of body-mass index (BMI), according to the study.

#glutamine #leanmass #inflammation

”Glutamine links obesity to inflammation in human white adipose tissue,” Paul Petrus, Simon Lecoutre, Lucile Dollet, Clotilde Wiel, André Sulen, Hui Gao, Beatriz Tavira, Jurga Laurencikiene, Olav Rooyackers, Antonio Checa, Iyadh Douagi, Craig E. Wheelock, Peter Arner, Mark McCarthy, Martin O. Bergo, Laurienne Edgar, Robin P. Choudhury, Myriam Aouadi, Anna Krookand Mikael Rydén, Cell Metabolism, online December 19, 2019. https://doi.org/10.1016/j.cmet.2019.11.019

Heart Failure improved with Antioxidant Combination

Heart Failure improved with Antioxidant Combination

Heart Failure improved with Antioxidant Combination

“””the measure of function in large blood vessels and of inflammation improved with treatment. Similarly, the presence of biologically available nitric oxide, a compound that helps blood vessels dilate, also increased.””

Over-the-counter Antioxidant Cocktail Improved Vascular Function in Certain Patients with Heart Failure – The American Physiological Society Press Release April 9, 2019

http://www.the-aps.org/mm/hp/Audiences/Public-Press/2019-22.html

Antioxidants and amino acids could play role in mental illness

Antioxidants and amino acids could play role in mental illness

The systematic review involved eight independent clinical trials of nutrient supplementation in 457 young people. The review primarily covered ‘first-episode psychosis’ (FEP) as well as schizophrenia and a myriad of other ailments associated with the two.

Adjunctive nutrients in first-episode psychosis: A systematic review of efficacy, tolerability and neurobiological mechanisms. Early Intervention in Psychiatry, 2018; DOI: 10.1111/eip.12544

High omega-6 levels protect greatly against premature death

High omega-6 levels protect greatly against premature death

Researchers discovered that the risk of premature death was 43% lower in the group with the highest level of Omega-6, when compared to the group with the lowest level.

Serum n–6 polyunsaturated fatty acids and risk of death: the Kuopio Ischaemic Heart Disease Risk Factor Study The American Journal of Clinical Nutrition, Volume 107, Issue 3, 1 March 2018, Pages 427–435, DOI:10.1093/ajcn/nqx063

Non-human sugar in biotech drugs causes inflammation

EEV: Since this initial release from 2010, we believe there has been absolutely no action

English: Anomeric configurations of Neu5Ac and...
English: Anomeric configurations of Neu5Ac and numbering scheme. (Photo credit: Wikipedia)

Public release date: 25-Jul-2010

– sugar molecule common to chimpanzees, gorillas and other mammals * but not found in humans * provokes a strong immune response in some people, likely worsening conditions in which chronic inflammation

The problem may also be exacerbated by the presence of Neu5Gc in drugs developed through recombinant biotechnology, some of which are actually used to treat inflammatory disorders

The presence of the non-human sialic acid sugar contaminant, called N-glycolyneuraminic acid or Neu5Gc, has long been known but ignored because it was believed healthy human immune systems did not react to it — “Now we know that to be untrue.”

– “It’s part of our diet, and especially abundant in red meat. We all develop antibodies to Neu5Gc

–  If there is a strong antibody response to diet-incorporated Neu5Gc, the resulting inflammation could cause harm to the person. This may partially explain associations between certain foods and increased risk of diseases associated with inflammation, such as cancer and heart attacks – diseases that are rare in other primates

Researchers at the University of California, San Diego School of Medicine have discovered that a kind of sugar molecule common to chimpanzees, gorillas and other mammals but not found in humans provokes a strong immune response in some people, likely worsening conditions in which chronic inflammation is a major issue Continue reading “Non-human sugar in biotech drugs causes inflammation”

173 Health Research Report 25 JAN 2010

 HRR

173

25 JAN 2014 /  White paper draft

Compiled by Ralph Turchiano

 

•        Detailed research references and further affiliations on each article are posted at http://www.healthreserachreport.me .

In this Issue:

  1. Study examines probiotic use in preventing gastrointestinal disorders in infants
  2. Altering the community of gut bacteria promotes health and increases lifespan
  3. Warning! Warning Labels Can Be Dangerous to Your Health
  4. Vitamin D supplements reduce pain in fibromyalgia sufferers
  5. Higher vitamin D levels associated with better cognition and mood in PD patients
  6. Melatonin may lower prostate cancer risk
  7. Ingredients in chocolate, tea and berries could guard against diabetes
  8. McMaster University researchers find fever-reducing medications may aid spread of influenza
  9. Can fish oil help preserve brain cells?
  10. Detecting Sickness By Smell
  11. More benefits emerging for one type of omega-3 fatty acid: DHA

Continue reading “173 Health Research Report 25 JAN 2010”

Olive oil component alleviates intestinal ischemia and reperfusion

Contact: Cody Mooneyhan cmooneyhan@faseb.org 301-634-7104 Federation of American Societies for Experimental Biology

New research published in the Journal of Leukocyte Biology shows that oleuropein aglycone, a polyphenol present in olive oil, reduces inflammation associated with intestinal ischemia and reperfusion injury in mice

Here’s another reason why you should include olive oil in your diet: A new research report published in the Journal of Leukocyte Biology suggests that at least one compound in olive oil significantly reduces intestinal ischemia (restricted blood supply) and the resulting reperfusion injury (tissue damage caused when blood supply returns). The compound, called “oleuropein aglycone,” is the most prominent polyphenol found in olive oil and could become a novel therapeutic target aimed at treating intestinal ischemia and reperfusion injury in humans. Ultimately, this research could lead to therapeutic benefits for patients with spinal cord injuries, arthritis and pleurisy, as well as those suffering from intestinal ischemia/reperfusion.

“The phenolic compounds of olive oil can reduce the secondary injury associated with intestinal damage,” said Salvatore Cuzzocrea, Ph.D., a senior researcher involved in the work from the Department of Biology and Environmental Sciences at the University of Messina in Messina, Italy. “Oleuropein aglycone may be useful in the therapy of inflammation-associated disease.”

To make this discovery, scientists used four groups of mice. The first group was subjected to intestinal ischemia by splanchnic arterial occlusion (SAO) followed by reperfusion. The second group was the same as the first but was also administered oleuropein aglycone. The third group of mice underwent identical surgical procedures except for SAO shock and was kept under anesthesia for the duration of the experiment. The last group was the same as the third, but was also given oleuropein aglycone. The histological structure of the gastrointestinal tract from the third group was typical of a normal architecture, but did not present any early inflammation. The ileum from animals subjected to intestinal ischemia/reperfusion injury (IRI) showed severe histological alteration with edema of the distal portion of the villi and the expression of pro-inflammatory cytokines, apoptosis and neutrophil infiltration were significantly increased. Oleuropein aglycone treated-mice showed reduced IRI-induced organ injury including a considerable reduction of inflammatory and apoptotic levels.

“Olive oil’s healing properties have been known for millennia,” said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology, “but until relatively recently, we have had few direct scientific insights into exactly how it works in the body. Not only does this report shed light on the molecular details of how olive oil may provide health benefits, but it may open new doors to enhancing treatments based on this discovery.”

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The Journal of Leukocyte Biology publishes peer-reviewed manuscripts on original investigations focusing on the cellular and molecular biology of leukocytes and on the origins, the developmental biology, biochemistry and functions of granulocytes, lymphocytes, mononuclear phagocytes and other cells involved in host defense and inflammation. The Journal of Leukocyte Biology is published by the Society for Leukocyte Biology.

Details: Michela Campolo, Rosanna Di Paola, Daniela Impellizzeri, Rosalia Crupi, Valeria Maria Morittu, Antonio Procopio, Enzo Perri, Domenico Britti, Angelo Peli, Emanuela Esposito, and Salvatore Cuzzocrea. Effects of a polyphenol present in olive oil, oleuropein aglycone, in a murine model of intestinal ischemia/reperfusion injury. J. Leukoc. Biol. February 2013 93:277-287; doi:10.1189/jlb.0712317 ; http://www.jleukbio.org/content/93/2/277.abstract.

Chromium picolinate may lessen inflammation in diabetic nephropathy

Contact: Donna Krupa DKrupa@the-aps.org 301-634-7209 American Physiological Society

Supplement linked to decreased protein in the urine of diabetic mice

Bethesda, Md. (September 22, 2010) – Taking chromium picolinate may help lessen inflammation associated with diabetic nephropathy (kidney disease), say researchers at the Medical College of Georgia in Augusta. In a study comparing diabetic mice treated with chromium picolinate with those that received placebo, the researchers found that mice who received the supplement had lower levels of albuminuria (protein in the urine), an indication of kidney disease.

The Study

To arrive at their conclusions, the researchers compared three groups of mice, one lean, healthy group and two groups genetically engineered to be obese and have diabetes. When the mice were 6 weeks old, the researchers separated them according to treatment plan. The healthy mice and one group of diabetic mice, the untreated diabetic group, were fed a regular rodent diet. The remaining group, the treated diabetic group, were fed a diet enriched with chromium picolinate.

Over the course of 6 months, the researchers measured glycemic control and albuminuria in all three groups. The untreated diabetic mice excreted nearly 10 times more albumin than the db/m mice, which was to be expected. However, the treated diabetic mice, who were fed the diet with chromium picolinate, excreted about half as much albumin compared to their untreated diabetic counterparts.

At the end of 6 months, the mice were euthanized and the researchers studied tissue samples from the mice’s kidneys. They found that the untreated diabetic mice had marked immunostaining for interleukin 6 (IL-6) and interleukin 17 (IL-17), two cytokines associated with inflammation. These mice also had moderate immunostaining for indolamine 2,3-dioxygenase (IDO), an immunoregulatory enzyme that modulates the production of IL-6 and IL-17. However, the treated diabetic mice had intense immunostaining for IDO but reduced IL-6 and IL-17 compared to the untreated diabetic group. The implication is that the chromium picolinate may have reduced inflammation in the treated diabetic group by affecting IDO, IL-6, and IL-7.

Mahmood Mozaffari, DMD, PhD, professor in the Medical College of Georgia Department of Oral Biology and lead author of the study, noted that the results are preliminary and that further studies are necessary to tease out the effects of chromium picolinate. He is particularly interested in the relationship between IDO and chromium picolinate because IDO is involved in the metabolism of tryptophan, an amino acid, and one of the by-products of that metabolism is picolinic acid.

“This clearly raises an important question for us as to whether our observations are related to the provision of picolinic acid from the chromium picolinate or whether the formulation [chromium picolinate], in and of itself, is mediating the effects.”

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NOTE TO EDITORS: Dr. Mozaffari discussed the study at the 2010 American Physiological Society conference, Inflammation, Immunity, and Cardiovascular Disease, in Westminster Colorado. To arrange an interview with him, please contact Donna Krupa at 301.634.7209 or dkrupa@the-aps.org.

Physiology is the study of how molecules, cells, tissues and organs function to create health or disease. The American Physiological Society (www.The-APS.org/press) has been an integral part of this discovery process since it was established in 1887.

Aspirin, Tylenol May Decrease Effectiveness of Vaccines: “if you block COX-1, you might be decreasing the amount of antibodies your body is producing”

2009 study posted for filing

Contact: Kelsey Jackson JacksonKN@missouri.edu 573-882-8353 University of Missouri-Columbia

Aspirin, tylenol may decrease effectiveness of vaccines

Mizzou scientists discover aspirin and Tylenol block enzymes that could inhibit vaccines

COLUMBIA, Mo. – With flu season in full swing and the threat of H1N1 looming, demand for vaccines is at an all-time high. Although those vaccines are expected to be effective, University of Missouri researchers have found further evidence that some over-the-counter drugs, such as aspirin and Tylenol, that inhibit certain enzymes could impact the effectiveness of vaccines.

“If you’re taking aspirin regularly, which many people do for cardiovascular treatment, or acetaminophen (Tylenol) for pain and fever and get a flu shot, there is a good chance that you won’t have a good antibody response,” said Charles Brown, associate professor of veterinary pathobiology in the MU College of Veterinary Medicine. “These drugs block the enzyme COX-1, which works in tissues throughout the body. We have found that if you block COX-1, you might be decreasing the amount of antibodies your body is producing, and you need high amounts of antibodies to be protected.”

COX enzymes play important roles in the regulation of the immune system. The role of these enzymes is not yet understood completely, and medications that inhibit them may have adverse side effects. Recent research has discovered that drugs that inhibit COX enzymes, such as COX-2, have an impact on the effectiveness of vaccines. Brown’s research indicates that inhibiting COX-1, which is present in tissues throughout the body, such as the brain or kidneys, could also impact vaccines’ effectiveness.

These MU researchers also are studying the regulation of inflammation and how that leads to the development or prevention of disease. Many diseases, such as arthritis, cardiovascular disease and diabetes, are all chronic inflammatory diseases. Contrary to previous beliefs, inflammation is generally a good thing that helps protect individuals from infection. Many of the non-steroidal drugs that treat inflammatory conditions reduce antibody responses, which are necessary for treating infections.

“So far, we’ve tested this on an animal model and have found that these non-steroidal drugs do inhibit vaccines, but the next step is to test it on humans,” Brown said. “If our results show that COX-1 inhibitors affect vaccines, the takeaway might be to not take drugs, such as aspirin, Tylenol and ibuprofen, for a couple weeks before and after you get a vaccine.”

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Brown’s research, “Cycloozygenase-1 Orchestrates Germinal Center Formation and Antibody Class-Switch via Regulation of IL-17,” has been published in The Journal of Immunology.

Oxidized form of Vitamin A, may bring relief for ulcerative colitis

2009 study posted for filing

Contact: Cody Mooneyhan
cmooneyhan@faseb.org
301-634-7104
Federation of American Societies for Experimental Biology

New research published in the Journal of Leukocyte Biology finds retinoic acid may alleviate ulcerative colitis and similar irritable bowel diseases

Here’s another reason why you should take your vitamins. A new research report appearing in the October 2009 print issue of the Journal of Leukocyte Biology (http://www.jleukbio.org) suggests that retinoic acid, the oxidized form of vitamin A, could be a beneficial treatment for people suffering from ulcerative colitis and other irritable bowel diseases. Specifically they found that retinoic acid helps suppress out-of-control inflammation, which is a hallmark of active ulcerative colitis.

“Pharmaceutical strategies based on this research may offer a promising alternative to our current approaches of managing immune diseases including, IBD, arthritis, multiple sclerosis, and so on,” Aiping Bai, a researcher involved in the work from Nanchang University in Nanchang City, China.

To make this discovery, Bai and colleagues conducted in vitro studies with human tissue and in vivo studies in mice. Both studies ultimately found that treatment with retinoic acid reduced the inflammation in the colon by increasing the expression of FOXP3, a gene involved with immune system responses, as well as decreasing the expression of IL-17, a cytokine believed to cause inflammation. Because many experts believe that IL-17 directly relates to the uncontrolled inflammation seen in ulcerative colitis and irritable bowel disease, the discovery that retinoic acid reduces IL-17’s ability to cause inflammation could accelerate the development of treatments for these chronic diseases.

“Runaway inflammation is serious problem, no matter where it occurs in the body, but in many instances, the root cause is a mystery,” said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. “This research helps scientists better understand what causes and controls inflammation in the colon, which in turn, helps lay the groundwork for new classes of drugs to treat this devastating condition.”

 

###

 

The Journal of Leukocyte Biology (http://www.jleukbio.org) publishes peer-reviewed manuscripts on original investigations focusing on the cellular and molecular biology of leukocytes and on the origins, the developmental biology, biochemistry and functions of granulocytes, lymphocytes, mononuclear phagocytes and other cells involved in host defense and inflammation. The Journal of Leukocyte Biology is published by the Society for Leukocyte Biology.

Details: Aiping Bai, Nonghua Lu, Yuan Guo, Zhanju Liu, Jiang Chen, and Zhikang Peng. All-trans retinoic acid down-regulates inflammatory responses by shifting the Treg/Th17 profile in human ulcerative and murine colitis. J Leukoc Biol 2009 86: 959� doi: doi:10.1189/jlb.0109006 ; http://www.jleukbio.org/cgi/content/abstract/86/4/959

Ginger causes ovarian cancer cells to die, U-M researchers find

2006 study posted for filing

Contact: Nicole Fawcett
nfawcett@umich.edu
734-764-2220
University of Michigan Health System

Cell studies show promise for ginger as potential ovarian cancer treatment

ANN ARBOR, Mich. — Ginger is known to ease nausea and control inflammation. But researchers at the University of Michigan Comprehensive Cancer Center are investigating a new use for this age-old remedy: treating ovarian cancer.

In laboratory studies, researchers found ginger caused ovarian cancer cells to die. Further, the way in which the cells died suggests ginger may avoid the problem common in ovarian cancer of cells becoming resistant to standard treatments.

The researchers are presenting their results in a poster session at the American Association for Cancer Research annual meeting.

Researchers used ginger powder, similar to what is sold at grocery stores, only a standardized research grade. The ginger powder was dissolved in solution and applied to ovarian cancer cell cultures. Ginger induced cell death in all the ovarian cancer cell lines tested.

Moreover, the researchers found that ginger caused two types of cell death. One type, known as apoptosis, results from cancer cells essentially committing suicide. The other type of cell death, called autophagy, results from cells digesting or attacking themselves.

“Most ovarian cancer patients develop recurrent disease that eventually becomes resistant to standard chemotherapy – which is associated with resistance to apoptosis. If ginger can cause autophagic cell death in addition to apoptosis, it may circumvent resistance to conventional chemotherapy,” says study author J. Rebecca Liu, M.D., assistant professor of obstetrics and gynecology at the U-M Medical School and a member of the U-M Comprehensive Cancer Center.

Study results are very preliminary, and researchers plan to test whether they can obtain similar results in animal studies. The appeal of ginger as a potential treatment for ovarian cancer is that it would have virtually no side effects and would be easy to administer as a capsule.

Ginger is effective at controlling inflammation, and inflammation contributes to the development of ovarian cancer cells. By halting the inflammatory reaction, the researchers suspect, ginger also stops cancer cells from growing.

“In multiple ovarian cancer cell lines, we found that ginger induced cell death at a similar or better rate than the platinum-based chemotherapy drugs typically used to treat ovarian cancer,” says Jennifer Rhode, M.D., a gynecologic oncology fellow at the U-M Medical School.

Liu’s lab is also looking at the effects on ovarian cancer of resveratrol, a substance found in red wine, and curcumin, the active ingredient in the curry spice turmeric. In addition, researchers at the U-M Comprehensive Cancer Center are investigating ginger to control nausea from chemotherapy and ginger to prevent colon cancer.

“Patients are using natural products either in place of or in conjunction with chemotherapy, and we don’t know if they work or how they work. We don’t know how these products interact with chemotherapy or other cancer treatments. There’s no good clinical data,” Liu says.

###

More than 20,000 women are expected to be diagnosed with ovarian cancer this year, and 15,000 will die from the disease, according to the American Cancer Society. For information about ovarian cancer, go to www.cancer.med.umich.edu/learn/ovarianinfo.htm or call the U-M Cancer AnswerLine at 800-865-1125.

In addition to Rhode and Liu, study authors are undergraduate student Jennifer Huang, research associates Sarah Fogoros and Lijun Tan, and Suzanna Zick, N.D., M.P.H., research investigator in family medicine.

Funding for the study was from the National Center for Complementary and Alternative Medicine, National Institutes of Health.

Reference: American Association for Cancer Research 97th annual meeting, April 1-5, 2006, Washington, D.C.

Antioxidant found in berries, other foods prevents UV skin damage that leads to wrinkles: ellagic acid,

2009 study posted for filing

Contact: Sylvia Wrobel
ebpress@gmail.com
770-722-0155
Federation of American Societies for Experimental Biology

Using a topical application of the antioxidant ellagic acid, researchers at Hallym University in the Republic of Korea markedly prevented collagen destruction and inflammatory response – major causes of wrinkles — in both human skin cells and the sensitive skin of hairless mice following continuing exposure to UV-B, the sun’s skin-damaging ultraviolet radioactive rays.

Ji-Young Bae, a graduate student in the laboratory of Dr. Young-Hee Kang, presented results of the two-part study on Tuesday, April 21, at the Experimental Biology 2009 meeting in New Orleans. The presentation was part of the scientific program of the American Society for Nutrition.

Ellagic acid is an antioxidant found in numerous fruits, vegetables and nuts, especially raspberries, strawberries, cranberries and pomegranates. Earlier studies have suggested it has a photoprotective effect.

But how? The Kang laboratory found that, in human skin cells, ellagic acid worked to protect against UV damage by blocking production of MMP (matrix metalloproteinase enzymes that break down collagen in damaged skin cells) and by reducing the expression of ICAM (a molecule involved in inflammation).

The scientists then turned to young (four weeks), male, hairless mice – genetically bred types of mice often used in dermatology studies because of the physiological similarities of their skin to that of humans. For eight weeks, the 12 mice were exposed to increasing ultraviolet radiation, such as that found in sunlight, three times a week, beginning at a level sufficient to cause redness or sunburn and increasing to a level that would have definitely caused minor skin damage to human skin.

During these eight weeks, half of the exposed mice were given daily 10 microM topical applications of ellagic acid on their skin surface, even on the days in which they did not receive UV exposure. The other mice, also exposed to UV light, did not receive ellagic acid. (Another six mice served as controls, with neither UV exposure nor ellagic acid.)

What happened? First, as expected, the mice exposed to UV radiation without the ellagic acid treatment developed wrinkles and thickening of the skin.

Second, as hypothesized, the exposed mice that received topical application of ellagic acid showed reduced wrinkle formation.

Third, as suggested in the study of human cells, the ellagic acid reduced inflammatory response and MMP secretion due to protection from the degradation of collagen. The ellagic acid also helped prevent an increase of epidermal thickness

The researchers say the results demonstrate that ellagic acid works to prevent wrinkle formation and photo-aging caused by UV destruction of collagen and inflammatory response.

 

###

 

In addition to Ji-Young Bae and Dr. Young-Hee Kang, co-authors were Jung-Suk Choi, Sang-Wook Kang, Dong Shoo Kim, and Jung Lye Kim. The research was supported by the Korea Research Foundation and Brain Korea 21.

 

Social contact can ease pain related to nerve damage, animal study suggests

Contact: Adam Hinzey
Adam.Hinzey@osumc.edu
Ohio State University

COLUMBUS, Ohio – Companionship has the potential to reduce pain linked to nerve damage, according to a new study.

Mice that were paired with a cage-mate showed lower pain responses and fewer signs of inflammation in their nervous system after undergoing surgery that affected their nerves than did isolated mice, suggesting that the social contact had both behavioral and physiological influences.

The social contact lowered the pain response and signs of inflammation even in animals that had experienced stress prior to the nerve injury.

These mice experienced a specific kind of nerve-related pain called allodynia, which is a withdrawal response to a stimulus that normally would not elicit a response – in this case, a light touch to the paw.

“If they were alone and had stress, the animals had increased inflammation and allodynia behavior,” said Adam Hinzey, a graduate student in neuroscience at Ohio State University and lead author of the study. “If the mice had a social partner, both allodynia and inflammation were reduced.”

More than 20 million Americans experience the nerve pain known as peripheral neuropathy as a consequence of diabetes or other disorders as well as trauma, including spinal cord injury. Few reliable treatments are available for this persistent pain.

“A better understanding of social interaction’s beneficial effects could lead to new therapies for this type of pain,” Hinzey said.

Hinzey described the research during a press conference Monday (10/15) in New Orleans at Neuroscience 2012, the annual meeting of the Society for Neuroscience.

In the study, researchers paired one group of mice with a single cage-mate for one week while other mice were kept socially isolated. For three days during this week, some mice from each group were exposed to brief stress while others remain nonstressed.

Researchers then performed a nerve surgery producing sensations that mimic neuropathic pain on one group of mice and a sham procedure that didn’t involve the nerves on a control group.

After determining a baseline response to a light touch to their paws, researchers tested all groups of mice behaviorally for a week after the surgery. Mice that had lived with a social partner, regardless of stress level, required a higher level of force before they showed a withdrawal response compared to isolated mice that were increasingly responsive to a lighter touch.

“Animals that were both stressed and isolated maintained a lower threshold – less force was needed to elicit a paw withdrawal response. Animals that were pair housed and not stressed withstood a significantly greater amount of force applied before they showed a paw withdrawal response,” Hinzey said. “Within animals that were stressed, pairing was able to increase the threshold required to see a withdrawal response.”

He and colleagues examined the animals’ brain and spinal cord tissue for gene activation affecting production of two proteins that serve as markers for inflammation. These cytokines, called interleukin-1 beta (IL-1B) and interleukin-6 (IL-6), are typically elevated in response to both injury and stress.

Compared to animals that received a sham procedure, isolated mice with nerve damage had much higher levels of IL-1B gene expression in their brain and spinal cord tissue. The researchers also observed a significant decrease in gene activity related to IL-6 production in the spinal cords of nonstressed animals compared to the mice that were stressed.

“We believe that socially isolated individuals are physiologically different from socially paired individuals, and that this difference seems to be related to inflammation,” said Courtney DeVries, professor of neuroscience at Ohio State and principal investigator on this work. “These data showed very nicely that the social environment is influencing not just behavior but really the physiological response to the nerve injury.”

###

This work was supported by funds from the National Institute of Nursing Research. Additional co-authors include Brant Jarrett and Kathleen Stuller of Ohio State’s Department of Neuroscience.

Contact: Adam Hinzey, Adam.Hinzey@osumc.edu

Written by Emily Caldwell, (614) 292-8310; Caldwell.151@osu.edu

(Hinzey will be at Neuroscience 2012 from Oct. 13-17; during this time, contact Hinzey via email or by calling Emily Caldwell at (614) 893-4261.)

Editor’s note: Hinzey will present his poster (No. 786.04) between 11 a.m. and noon (CT) Wednesday (10/17) in Hall F-J at the Ernest N. Morial Convention Center in New Orleans.

Caffeine may block inflammation linked to mild cognitive impairment

Contact: Phyllis Picklesimer p-pickle@illinois.edu 217-244-2827 University of Illinois College of Agricultural, Consumer and Environmental Sciences

URBANA – Recent studies have linked caffeine consumption to a reduced risk of Alzheimer’s disease, and a new University of Illinois study may be able to explain how this happens.

“We have discovered a novel signal that activates the brain-based inflammation associated with neurodegenerative diseases, and caffeine appears to block its activity. This discovery may eventually lead to drugs that could reverse or inhibit mild cognitive impairment,” said Gregory Freund, a professor in the U of I’s College of Medicine and a member of the U of I’s Division of Nutritional Sciences.

Freund’s team examined the effects of caffeine on memory formation in two groups of mice—one group given caffeine, the other receiving none. The two groups were then exposed to hypoxia, simulating what happens in the brain during an interruption of breathing or blood flow, and then allowed to recover.

The caffeine-treated mice recovered their ability to form a new memory 33 percent faster than the non-caffeine-treated mice. In fact, caffeine had the same anti-inflammatory effect as blocking IL-1 signaling. IL-1 is a critical player in the inflammation associated with many neurodegenerative diseases, he said.

“It’s not surprising that the insult to the brain that the mice experienced would cause learning memory to be impaired. But how does that occur?” he wondered.

The scientists noted that the hypoxic episode triggered the release of adenosine by brain cells.

“Your cells are little powerhouses, and they run on a fuel called ATP that’s made up of molecules of adenosine. When there’s damage to a cell, adenosine is released,” he said.

Just as gasoline leaking out of a tank poses a danger to everything around it, adenosine leaking out of a cell poses a danger to its environment, he noted.

The extracellular adenosine activates the enzyme caspase-1, which triggers production of the cytokine IL-1β, a critical player in inflammation, he said.

“But caffeine blocks all the activity of adenosine and inhibits caspase-1 and the inflammation that comes with it, limiting damage to the brain and protecting it from further injury,” he added.

Caffeine’s ability to block adenosine receptors has been linked to cognitive improvement in certain neurodegenerative diseases and as a protectant against Alzheimer’s disease, he said.

“We feel that our foot is in the door now, and this research may lead to a way to reverse early cognitive impairment in the brain. We already have drugs that target certain adenosine receptors. Our work now is to determine which receptor is the most important and use a specific antagonist to that receptor,” he said.

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The study appears in the Journal of Neuroscience and can be viewed online at http://www.jneurosci.org/content/32/40/13945.full. Co-authors are Gabriel Chiu, Diptaman Chatterjee, Patrick Darmody, John Walsh, Daryl Meling, and Rodney Johnson, all of the U of I. Funding for the study was provided by the National Institutes of Health.

Zinc deficiency mechanism linked to aging, multiple diseases: animals given about 10 times their dietary requirement for zinc, the biomarkers of inflammation were restored to those of young animals.

10-1-12

Media Release

Zinc deficiency mechanism linked to aging, multiple diseases

CORVALLIS, Ore. – A new study has outlined for the first time a biological mechanism by which zinc deficiency can develop with age, leading to a decline of the immune system and increased inflammation associated with many health problems, including cancer, heart disease, autoimmune disease and diabetes.

The research was done by scientists in the Linus Pauling Institute at Oregon State University and the OSU College of Public Health and Human Sciences. It suggests that it’s especially important for elderly people to get adequate dietary intake of zinc, since they may need more of it at this life stage when their ability to absorb it is declining.

About 40 percent of elderly Americans and as many as two billion people around the world have diets that are deficient in this important, but often underappreciated micronutrient, experts say.

The study was published in the Journal of Nutritional Biochemistry, based on findings with laboratory animals. It found that zinc transporters were significantly dysregulated in old animals. They showed signs of zinc deficiency and had an enhanced inflammatory response even though their diet supposedly contained adequate amounts of zinc.

When the animals were given about 10 times their dietary requirement for zinc, the biomarkers of inflammation were restored to those of young animals.

“The elderly are the fastest growing population in the U.S. and are highly vulnerable to zinc deficiency,” said Emily Ho, an LPI principal investigator and associate professor in OSU School of Biological and Population Health Sciences. “They don’t consume enough of this nutrient and don’t absorb it very well.”

“We’ve previously shown in both animal and human studies that zinc deficiency can cause DNA damage, and this new work shows how it can help lead to systemic inflammation,” Ho said.

“Some inflammation is normal, a part of immune defense, wound healing and other functions,” she said. “But in excess, it’s been associated with almost every degenerative disease you can think of, including cancer and heart disease. It appears to be a significant factor in the diseases that most people die from.”

As a result of this and what is now know about zinc absorption in the elderly, Ho said that she would recommend all senior citizens take a dietary supplement that includes the full RDA for zinc, which is 11 milligrams a day for men and 8 milligrams for women. Zinc can be obtained in the diet from seafood and meats, but it’s more difficult to absorb from grains and vegetables – a particular concern for vegetarians.

“We found that the mechanisms to transport zinc are disrupted by age-related epigenetic changes,” said Carmen Wong, an OSU research associate and co-author of this study. “This can cause an increase in DNA methylation and histone modifications that are related to disease processes, especially cancer. Immune system cells are also particularly vulnerable to zinc deficiency.”

Research at OSU and elsewhere has shown that zinc is essential to protect against oxidative stress and help repair DNA damage. In zinc deficiency, the risk of which has been shown to increase with age, the body’s ability to repair genetic damage may be decreasing even as the amount of damage is going up.

Medical tests to determine zinc deficiency are rarely done, scientists say, and are not particularly accurate even if they are done. The best approach is to assure adequate intake of the nutrient through diet or supplements, they said, especially in the elderly.

Even though elderly people have less success in absorbing zinc, the official RDA for them is the same as in younger adults. That issue should be examined more closely, Ho said.

Levels of zinc intake above 40 milligrams per day should be avoided, researchers said, because at very high levels they can interfere with absorption of other necessary nutrients, including iron and copper.

These studies were supported by the National Institutes of Health and other agencies.

 

About the Linus Pauling Institute: The Linus Pauling Institute at OSU is a world leader in the study of micronutrients and their role in promoting optimum health or preventing and treating disease. Major areas of research include heart disease, cancer, aging and neurodegenerative disease.

Plant flavonoid found to reduce inflammatory response in the brain: luteolin

Contact: Diana Yates
diya@illinois.edu
217-333-5802
University of Illinois at Urbana-Champaign

IMAGE:Animal sciences professor Rodney Johnson, and graduate student Saebyeol Jang found that a plant flavonoid, luteolin, inhibited a key pathway in the inflammatory response of microglia.

Click here for more information. 

Researchers at the University of Illinois report this week that a plant compound found in abundance in celery and green peppers can disrupt a key component of the inflammatory response in the brain. The findings have implications for research on aging and diseases such as Alzheimer’s and multiple sclerosis.

The study appears this week in Proceedings of the National Academy of Sciences.

Inflammation can be a blessing or a blight. It is a critical part of the body’s immune response that in normal circumstances reduces injury and promotes healing. When it goes awry, however, the inflammatory response can lead to serious physical and mental problems.

Inflammation plays a key role in many neurodegenerative diseases and also is implicated in the cognitive and behavioral impairments seen in aging.

The new study looked at  (LOO-tee-OH-lin), a plant flavonoid known to impede the inflammatory response in several types of cells outside the central nervous system. The purpose of the study was to determine if luteolin could also reduce inflammation in the brain, said animal sciences professor and principal investigator Rodney Johnson.

“One of the questions we were interested in is whether something like luteolin, or other bioactive food components, can be used to mitigate age-associated inflammation and therefore improve cognitive function and avoid some of the cognitive deficits that occur in aging,” Johnson said.

The researchers first studied the effect of luteolin on microglia. These brain cells are a key component of the immune defense. When infection occurs anywhere in the body, microglia respond by producing inflammatory cytokines, chemical messengers that act in the brain to orchestrate a whole-body response that helps fight the invading microorganism.

This response is associated with many of the most obvious symptoms of illness: sleepiness, loss of appetite, fever and lethargy, and sometimes a temporary diminishment of learning and memory. Neuroinflammation can also lead some neurons to self-destruct, with potentially disastrous consequences if it goes too far.

Graduate research assistant Saebyeol Jang studied the inflammatory response in microglial cells. She spurred inflammation by exposing the cells to lipopolysaccharide (LPS), a component of the cell wall of many common bacteria.

Those cells that were also exposed to luteolin showed a significantly diminished inflammatory response. Jang showed that luteolin was shutting down production of a key cytokine in the inflammatory pathway, interleukin-6 (IL-6). The effects of luteolin exposure were dramatic, resulting in as much as a 90 percent drop in IL-6 production in the LPS-treated cells.

“This was just about as potent an inhibition as anything we had seen previously,” Johnson said.

But how was luteolin inhibiting production of IL-6″

Jang began by looking at a class of proteins involved in intracellular signaling, called transcription factors, which bind to specific “promoter” regions on DNA and increase their transcription into RNA and translation into proteins.

Using electromobility shift assays, which measure the binding of transcription factors to DNA promoters, Jang eventually determined that luteolin inhibited IL-6 production by preventing activator protein-1 (AP-1) from binding the IL-6 promoter.

AP-1 is in turn activated by JNK, an upstream protein kinase. Jang found that luteolin inhibited JNK phosphorylation in microglial cell culture. The failure of the JNK to activate the AP-1 transcription factor prevented it from binding to the promoter region on the IL-6 gene and transcription came to a halt.

To see if luteolin might have a similar effect in vivo, the researchers gave mice luteolin-laced drinking water for 21 days before injecting the mice with LPS.

Those mice that were fed luteolin had significantly lower levels of IL-6 in their blood plasma four hours after injection with the LPS. Luteolin also decreased LPS-induced transcription of IL-6 in the hippocampus, a brain region that is critical to spatial learning and memory.

The findings indicate a possible role for luteolin or other bioactive compounds in treating neuroinflammation, Johnson said.

“It might be possible to use flavonoids to inhibit JNK and mitigate inflammatory reactions in the brain,” he said. “Inflammatory cytokines such as interleukin-6 are very well known to inhibit certain types of learning and memory that are under the control of the hippocampus, and the hippocampus is also very vulnerable to the insults of aging,” he said. “If you had the potential to decrease the production of inflammatory cytokines in the brain you could potentially limit the cognitive deficits that result.”

 

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Editor’s note: To reach Rodney Johnson, call 217-333-2118; e-mail: rwjohn@uiuc.edu.

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Saturated Fats encourage the growth and invasiveness of harmful microbiota: Unsaturated fats—actually have strong antimicrobial properties

Why some fats are worse than others

All dietary fats are not created equal. Some types of fats have been linked to ailments like heart disease and diabetes, while others, like those often found in plants and fish, have well documented health benefits.

 

So why do our bodies respond so destructively to some fats but not others?

 

A new hypothesis described in latest issue of The Quarterly Review of Biology suggests the answer may lie in how different fats interact with the microbes in our guts. According to researchers from the University of New Mexico and Northwestern University, some fats may encourage the growth of harmful bacteria in the digestive system. Our bodies have evolved to recognize those fats and launch an immune response to preempt the impeding changes in harmful bacteria. The result is low-level inflammation that, over the long term, causes chronic disease.

 

“Although the inflammatory effects of [fats] are well documented, it is less well appreciated that they also influence bacterial survival and proliferation in the gastrointestinal tract,” write the researchers, led by Joe Alcock, of the University of New Mexico Department of Emergency Medicine and VA Medical Center.

 

Some fats—mostly unsaturated fats—actually have strong antimicrobial properties. They react chemically with bacterial cell membranes, weakening them. “If you expose unsaturated fats on bacteria, the bacteria have a tendency to lyse. The combination of long chain unsaturated fats, especially omega-3 fatty acids, and innate host defenses like gastric acid and antimicrobial peptides, is particularly lethal to pathogenic bacteria,” Alcock said. Saturated fats on the other hand generally lack those antimicrobial properties, and in fact can provide a carbon source that bacteria need to grow and flourish.

 

And it’s these differing microbial effects, Alcock believes, that are at the root of why some fats are inflammatory and some aren’t. To test that notion, the researchers poured through years of research on both the microbial effects of fats and their inflammatory effects.

 

“We found a highly significant relationship between those fats that had antimicrobial properties and those that had anti-inflammatory properties,” Alcock said. “Fats that lack antimicrobial properties tended to be pro-inflammatory. It was a very, very strong relationship.”

 

In a sense, the researchers say, the presence of saturated fats sets off an “early warning system” in the body. When fats that encourage bacterial growth are present, the body prepares for unwelcome microbial guests with an inflammatory immune response. And while that response may help fend off infection in the short term, the constant presence of such fats could cause the body to spiral into diseases related to inflammation, like heart disease.

 

The researchers caution that while this hypothesis is well supported by current data, there’s much more research to be done.

 

“We have a pretty good idea that eating fatty foods encourages the growth and invasiveness of harmful microbiota and we know that certain fats kill off these potentially harmful species,” Alcock said. “But we’re making a bit of a leap from the Petri dish to the whole organism.”

 

“We don’t intend this to be the final word. Rather it’s a tool to generate additional hypotheses that can be tested.”

Purple periwinkles battle inflammatory diseases ( COPD Treatment Breakthrough )

Repost from 2010…Breakthrough treatment completely ignored

Natural supplement boasts excellent safety

A widely and safely used plant extract acts as a novel anti-inflammatory agent that may one day be used for the treatment of chronic obstructive pulmonary disease, or COPD, as well as other inflammatory conditions. There is an urgent need for new therapies for the treatment of chronic inflammatory diseases, such as COPD, otitis media (ear infection), and atherosclerosis (chronic inflammation in the walls of arteries), because the most effective and commonly used agents – steroids – often cause serious side effects, such as liver damage, which prevent long-term use. 

In a study published today in the Proceedings of the National Academy of Sciences, researchers at the University of Rochester Medical Center were the first to find that vinpocetine, a natural product derived from the periwinkle plant, acts as a potent anti-inflammatory agent when tested in a mouse model of lung inflammation, as well as several other types of human cells.  Results of the study show that vinpocetine greatly reduces inflammation, and, unlike steroids, does not cause severe side effects.

“What is extremely exciting and promising about these findings is vinpocetine’s excellent safety profile,” said Chen Yan, Ph.D., associate professor within the Aab Cardiovascular Research Institute at the Medical Center and a senior author of the study. “Previously, most drugs tested in this area have failed, not because of a lack of efficacy, but because of safety issues. We’re very encouraged by these results and believe vinpocetine has great potential for the treatment of COPD and other inflammatory diseases.”

Vinpocetine is a well-known natural product that was originally discovered nearly 30 years ago and is currently used as a dietary supplement for the prevention and treatment of cognitive disorders, such as stroke and memory loss, in Europe, Japan and China. The therapy has no evidence of toxicity or noticeable side effects in human patients. Scientists at the University of Rochester hope to reposition this compound as an anti-inflammatory agent for the treatment of COPD, and potentially other inflammatory conditions, such as asthma, otitis media, rheumatoid arthritis, atherosclerosis and psoriasis in the future.

While steroids successfully combat inflammation, patients often pay a high price when it comes to side effects. Steroids can cause liver damage, and can also suppress the immune system, increasing the likelihood of infections. With such a high risk profile, steroids are usually only used for a short period of time, which is problematic when treating chronic diseases.

In managing chronic conditions such as COPD, it is crucial to have a therapy that can be used safely over the long term,” said Jian-Dong Li, M.D., Ph.D., professor in the Department of Microbiology and Immunology at the University of Rochester Medical Center and a senior author of the study. “There is a great need for a drug like vinpocetine, because patients currently have no good options when it comes to long-term care.” 

Vinpocetine decreases inflammation by targeting the activity of a specific enzyme, known as IKK. IKK is responsible for regulating inflammation, and does so through the activation of a key protein, nuclear-factor kappaB (NF-κB).  By directly inhibiting IKK, vinpocetine is able to switch off NF-κB, which normally produces pro-inflammatory molecules that cause inflammation. Halting the activity of NF-κB ultimately reduces inflammation.

“Inflammation is a hallmark of a wide range of human diseases, so there is great potential for vinpocetine to be used for several indications,” said Bradford C. Berk, M.D., Ph.D., CEO of the University of Rochester Medical Center and co-author of the study. “Given vinpocetine’s efficacy and solid safety profile, we believe there is great potential to bring this drug to market.”

Repositioning a therapy – taking a known compound that has been used safely in humans and testing it for a new application – can be an effective way to bring new therapies to market more quickly than starting the discovery process from scratch.

Inflammatory diseases are a major cause of illness worldwide. For example, chronic obstructive pulmonary disease is the fourth leading cause of death in the United States. In people with COPD, airflow is blocked due to chronic bronchitis or emphysema, making it increasingly difficult to breathe. Most COPD is caused by long-term smoking, although genetics may play a role as well. Approximately 13.5 million people in the United States are diagnosed with COPD each year, and in 2004 the annual cost of the disease was $37.2 billion.

Understanding the links between inflammation and chronic disease (NC)

Early exposure to microbes reduces inflammation related to chronic disease later

EVANSTON, Ill. — American parents may want to think again about how much they want to protect their children from everyday germs.

A new Northwestern University study done in lowland Ecuador remarkably finds no evidence of chronic low-grade inflammation — associated with diseases of aging like cardiovascular disease, diabetes and dementia.

In contrast, about one-third of adults in the United States have chronically elevated C-reactive protein (CRP). Acute elevations in CRP – a protein in the blood whose levels rise as part of the inflammatory response – are important for protecting us against infectious disease. But when CRP is chronically produced, it is associated with chronic diseases.

“In other words, CRP goes up when you need it, but it is almost undetectable when you don’t, after the infection resolves,” said Thomas W. McDade, professor of anthropology at Northwestern and faculty fellow at the university’s Institute for Policy Research. “This is a pretty remarkable finding, and very different from prior research in the U.S., where lots of people tend to have chronically elevated CRP, probably putting them at higher risk for chronic disease.”

McDade said the findings build on his previous research in the Philippines, which found that higher levels of microbial exposure in infancy were associated with lower CRP as an adult. Similar exposures during infancy in lowland Ecuador, where rates of infectious disease continue to be high, may have a lasting effect on the pattern of inflammation in adulthood.

“In my mind the study underscores the value of an ecological approach to research on the immune system, and it may have significant implications for our understanding of the links between inflammation and chronic disease,” McDade said. “This may be particularly important since nearly three-quarters of all deaths due to cardiovascular disease globally now occur in low- and middle-income nations like the Philippines and Ecuador.”

The new research, which was conducted as part of the Shuar Health and Life History Project (http://www.bonesandbehavior.org/shuar/), suggests that higher levels of exposure to infectious microbes early in life may change how we regulate inflammation as adults in ways that prevent chronic inflammation from emerging. Infectious microbes have been part of the human ecology for millennia, and it is only recently that more hygienic environments in affluent industrialized settings have substantially reduced the level and diversity of exposure.

A growing body of research has shown that higher levels of chronic inflammation are associated with diseases of aging like cardiovascular disease, diabetes and dementia. But current research is based almost exclusively on people living in affluent industrialized countries like the United States.

“We simply do not know what chronic inflammation looks like in places like the Ecuadorian Amazon and other parts of the world where infectious diseases are more common,” McDade said.

As a result, McDade, director of the Lab for Human Biology Research and director of Cells to Society (C2S): The Center on Social Disparities and Health, and collaborators at the University of Oregon set out to investigate what factors in the environment and during development influence how people regulate inflammation as adults. The study was conducted in lowland Ecuador – in a group of 52 adults between the ages of 18 and 49.

Based on current clinical criteria, McDade and colleagues did not find a single case of chronic low-grade inflammation among adults living in the Ecuadorian Amazon. McDade said people in these places are still dying of diseases such as cardiovascular disease, but probably not through processes that involve inflammation.

In terms of population health, McDade said these findings suggest that the association between inflammation and cardiovascular disease frequently reported in the United States may only apply in ecological settings characterized by low levels of exposure to infectious disease.

“It builds on research on chronic inflammation and cardiovascular disease in the U.S. and other affluent, industrialized settings and suggests that patterns seen here may not apply globally,” McDade said. “It also suggests that the levels of chronic inflammation we see in the U.S. are not universal, and may be a product of epidemiological transitions that have lowered our level of exposure to infectious microbe

A Common Microbe Could Help To Trigger Alzheimers

 

A COMMON microbe could help to trigger Alzheimer’s disease, say researchers in the US. If true, their controversial claim could turn the multimillion-dollar field of Alzheimer’s research on its head and force a rethink on how to prevent the disease.

The microbe in question is Chlamydia pneumoniae, which is spread by coughs and sneezes. By the age of 20, half the population have been infected with C. pneumoniae, and the likelihood of being infected increases with age. The bacterium has already been accused of triggering atherosclerosis-blocked arteries that can lead to heart attacks (“Can you catch a heart attack?”, New Scientist, 8 June 1996, p 38).

Alan Hudson at Wayne State University in Detroit and his colleagues did postmortems on the brains of 19 Alzheimer’s patients and 19 people of the same age who had died of other causes. They found signs of C. pneumoniae in 17 of the Alzheimer’s sufferers, in the hippocampus and temporal cortex. These are the parts of the brain which usually sustain most damage in Alzheimer’s disease. Unaffected areas of the brain were much less likely to harbour the bacterium. The bacterium turned up in the brain of only one of the non-Alzheimer’s patients.

The team also managed to culture the microbe from two of the affected brains, showing that the organism was still alive rather than a long-dead bystander (Medical Microbiology and Immunology, vol 187, p 23).

C. pneumoniae’s presence in the diseased brains does not mean that it cause Alzheimer’s, the scientists stress. But they think the bacterium may at least be a risk factor. Chlamydia bacteria do cause inflammation when they attack other parts of the body. And the brains of people with Alzheimer’s are inflamed and contain high levels of messenger chemicals called cytokines, which trigger inflammation.

Hudson says the bacterium infects microglia and astroglia, the cerebral cousins of scavenger cells called macrophages, and this produces inflammatory cytokines. “It seems reasonably likely that C. pneumoniae could be causing the inflammation,” says Hudson.

Author: Phyllida Brown New Scientist issue 15th August 1998, page 24

PLEASE MENTION NEW SCIENTIST AS THE SOURCE OF THIS ARTICLE