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    You are here : Home » MS Research News » New Discoveries » Mycoplasmas And Bacteria

    Mycoplasmas And Bacteria

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    Factors from common human bacteria may trigger multiple sclerosis

    Porphyromas gingivalisCurrent research suggests that a common oral bacterium may exacerbate autoimmune disease. The related report by Nichols et al, "Unique Lipids from a Common Human Bacterium Represent a New Class of TLR2 Ligands Capable of Enhancing Autoimmunity," appears in the December 2009 issue of The American Journal of Pathology.

    Multiple sclerosis (MS), a disease where the immune system attacks the brain and spinal cord, affects nearly 1 in 700 people in the United States. Patients with multiple sclerosis have a variety of neurological symptoms, including muscle weakness, difficulty in moving, and difficulty in speech.

    Porphyromas gingivalis, a common oral bacterium in humans, produces a unique type of lipid, phosphorylated dihydroceramides (DHCs), which enhance inflammatory responses. These lipids are also likely produced by bacteria found in other parts of the body including the gastrointestinal tract. To determine if these lipids accentuate immune-mediated damage in autoimmune disease, researchers led by Robert B. Clark and Frank C. Nichols of the University of Connecticut Health Center administered phosphorylated DHCs in a mouse model of MS.

    The severity of disease was significantly enhanced by the addition of these lipids in a manner that was dependent on activation of the immune system. These data suggest that phosphorylated DHCs from bacteria commonly found in humans may trigger or increase the severity of autoimmune diseases such as multiple sclerosis.

    The authors state that "while it is clear that the immune system in most individuals has the potential to attack self-tissues, the "tipping" factors that initiate and propagate autoimmune diseases such as multiple sclerosis in only a subset of individuals remain unknown. Overall, [their] results represent the first description that phosphorylated DHCs derived from common human bacteria are capable of enhancing autoimmune disease." Thus, these lipids may function as "tipping" factors, playing a previously unrecognized role in initiating or exacerbating human autoimmune diseases.

    In future studies, Dr. Clark and colleagues plan to characterize the effects of phosphorylated DHCs on specific cells of the immune system and to identify how and where these lipids are deposited in tissues throughout the body. In addition to the role of these lipids in triggering and worsening MS, the authors believe that phosphorylated DHCs may have the potential to serve both as new markers of MS disease activity and as new targets for therapeutic intervention.

    Source: Scinece Codex (24/11/09)

    'Hairy’ microbe spurs immune response

    Hairy BacteriaScientists have identified a bizarre-looking microbial species that can single-handedly kick start the production of specialized immune cells in mice. The finding could point to a similar phenomenon in humans, helping researchers understand how gut-dwelling bacteria protect us from pathogenic bacteria, such as virulent strains of E. coli.

    The study, published in the Oct. 30 issue of Cell, also supports the idea that specific bacteria may act like neighborhood watchdogs at key locations within the small intestine, where they sense the local microbial community and sound the alarm if something seems amiss.

    Distinguished by long hair-like filaments, “these bacteria are the most astounding things I’ve ever seen,” says Dan Littman, the Helen L. and Martin S. Kimmel Professor of Molecular Immunology at New York University and a Howard Hughes Medical Institute Investigator.

    Co-led by Littman’s lab, the collaboration with researchers in Japan, California, and Massachusetts zeroed in on a little-known microbe named segmented filamentous bacterium, or SFB. In mice raised under germ-free conditions, the scientists found that adding SFB was sufficient to trigger the appearance of specialized T helper cells known as Th17 cells.

    These immune specialists, in turn, can send signals that tell epithelial cells lining the small intestine to increase their output of molecules targeting selected microbes.

    For the study’s mice, the infection-fighting response was enough to ward off the pathogen Citrobacter rodentium, considered a good model for the type of disease-causing E. coli found in contaminated foods like spinach or ground beef. Without SFB to protect them, mice infected with Citrobacter rodentium became ill before recovering.

    In the same way, commensal microbes—beneficial bacteria—could decrease our susceptibility to various pathogenic invaders. “So you can immediately see some practical application of this, if one can mimic the presence of these commensal bacteria to strengthen resistance to pathogenic microbes,” Littman says.

    Thanks to rapid progress in the field of genomics, he expects the entire DNA sequence of the SFB species to be completed within a few months. Armed with the sequence, researchers could focus on specific proteins.

    “For example, can we identify a protein that, when we inject it into an epithelial cell, sets off in motion the whole pathway to make Th17 cells?” he says. “By knowing how to do this, you may be able to give people a peptide or a compound that induces Th17 cells by mimicking the bacterial product, and in that way either protect or ameliorate the effect of the infection.”

    Too much Th17 cell activation, however, can lead to harmful inflammation, Littman says. Excessive induction by specific microbes in the gut, then, could contribute to autoimmune diseases such as rheumatoid arthritis, psoriasis, Crohn’s disease, and possibly even multiple sclerosis.

    The study was supported by fellowships from the Crohn’s and Colitis Foundation of America and the Cancer Research Institute, and by grants from the National Institutes of Health; the Japan Science and Technology Agency’s PRESTO Program; the Ministry of Education, Culture, Sports, Science and Technology in Japan; the Senri Life Science Foundation; and the Naito Foundation.

    Source: Futurity.org © 2009 Futurity.org (16/10/09)

    NUIG lecturer leads Multiple Sclerosis research

    A major international research project into the possible causes of Multiple Sclerosis (MS) is being led by NUI Galway lecturer Dr. Thomas Barry, at the Department of Microbiology

    The joint molecular and clinical exploration of mycoplasmas and other bacteria that may play key roles in triggering MS, is being funded by the National Multiple Sclerosis Society New York.

    Neurology Professor Edward Hogan of NUI Galway and the Institute of Molecular Medicine and Genetics, Augusta, Georgia, USA will also be involved in the research.

    Source: Galway News - The Connacht Tribune Ltd. (17/07/07)

    © Multiple Sclerosis Resource Centre

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