Wednesday, 16 July 2014

Microbiome makes regulation

Wang Y, Begum-Haque S, Telesford KM, Ochoa-Repáraz J, Christy M, Kasper EJ, Kasper DL, Robson SC, Kasper LH A commensal bacterial product elicits and modulates migratory capacity of CD39+ CD4 T regulatory subsets in the suppression of neuroinflammation.Gut Microbes. 2014 Jul;5(4). [Epub ahead of print]

Tolerance established by host-commensal interactions regulates host immunity at both local mucosal and systemic levels. The intestinal commensal strain Bacteroides fragilis elicits immune tolerance, at least in part, via the expression capsular polysaccharide A (PSA). How such niche-specific commensal microbial elements regulate extra-intestinal immune responses, as in the brain, remains largely unknown. We have recently shown that oral treatment with PSA suppresses neuro-inflammation elicited during experimental autoimmune encephalomyelitis (EAE), an animal model formultiple sclerosis. This protection is dependent upon the expansion of immune-regulatory CD4 T cells (Treg) expressing CD39, an ectonucleotidase. Here, we further show that CD39 modulation of purinergic signals enhances migratory phenotypes of both total CD4 T cells and Foxp3+ CD4 Tregs at central nervous system (CNS) lymphoid-draining sites in EAE in vivo and promotes their migration in vitro. These changes are noted during PSA treatment, which leads to heightened accumulation of CD39+ CD4 Tregs in the CNS. Deficiency of CD39 abrogates accumulation of Treg during EAE, and is accompanied by elevated Th1/Th17 signals in the CNS and in gut-associated lymphoid tissues. Our results demonstrate that immune-modulatory commensal bacterial products impact the migratory patterns of CD4 Treg during CNS autoimmunity via the regulation of CD39. These observations provide clues as to how intestinal commensal microbiome is able to modulate Treg functions and impact host immunity in the distal site.
The microbiome or gut bacteria is a hot topic in immunology as it is thought that gut bacteria can make subtle changes in the way that your immune response develops such that it could be the difference between health and disease. So in this study a bacterial protein produced by bacteria found in the gut, is claimed to produce immune signals that turn off the immune response by promoting T regulatory T cells. These migrate and accumulate in the CNS. There is an immense amount of research going on around this subject, which will no doubt spawn clinical trials.

However it is something that rogues can easily latch onto, so you will be sold a few days in a health farm whilst your bacteria are cleansed and replaced by friendly bacteria. This needs no neuros so mark my words these clinics will spring up to take your money. Whilst there may be some merit in some conditions, its value in MS is unproven and so be warned.

1 comment:

  1. I wonder if there is any relationship or common thread of microbiome dysfunction in this research article and prior research articles?

    http://www.sciencedaily.com/releases/2011/10/111027112520.htm

    http://www.sciencedaily.com/releases/2014/01/140128153940.htm

    microbiome possible avenue for pathogens in another illness.
    http://www.microbediscovery.org/blog/2014/05/19/dr-ian-lipkin-blog-part-1-of-9/

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