Gut flora making susceptibility

Stanisavljević S, Lukić J, Soković S, Mihajlovic S, Mostarica Stojković M, Miljković D, Golić N.Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats. Front Microbiol. 2016;7:2005. doi: 10.3389/fmicb.2016.02005.

Multiple sclerosis is a chronic inflammatory disease of the central nervous system (CNS). It is widely accepted that autoimmune response against the antigens of the CNS is the essential pathogenic force in the disease. It has recently become increasingly appreciated that activated encephalitogenic cells tend to migrate toward gut associated lymphoid tissues (GALTs) and that interrupted balance between regulatory and inflammatory immunity within the GALT might have decisive role in the initiation and propagation of the CNS autoimmunity. Gut microbiota composition and function has the major impact on the balance in the GALT. Thus, our aim was to perform analyses of gut microbiota in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Albino Oxford (AO) rats that are highly resistant to EAE induction and Dark Agouti (DA) rats that develop EAE after mild immunization were compared for gut microbiota composition in different phases after EAE induction. 

Microbial analyses of the genus Lactobacillus and related lactic acid bacteria showed higher diversity of Lactobacillus spp. in EAE-resistant AO rats, while some members of Firmicutes and Proteobacteria (Undibacterium oligocarboniphilum) were detected only in faeces of DA rats at the peak of the disease (between 13 and 16 days after induction). Interestingly, in contrast to our previous study where Turicibacter sp. was found exclusively in non-
DA rats that remained healthy 16 days after induction, as well as in four of 12 DA rats at the peak of the disease. Similar observation was obtained for the members of Lachnospiraceae. Further, production of a typical regulatory cytokine interleukin-10 was compared in GALT cells of AO and DA rats, and higher production was observed in DA rats. Our data contribute to the idea that gut microbiota and GALT considerably influence multiple sclerosis pathogenesis.

In this paper they look at the bactrial flora in the gut of different strains of rat and infere thtat they influence suceptibility. This is the mantra for the microbiomome story. There is also an implication that this is one of the reasons why a resistant strain does not develop disease. To make this claim they would need to change the microbiome and make the resitant susceptible and the susceptible resistant. I doubt this would really happen as genetics has already been shown to be a key player in this. Anyway as you rush for that feacal transplant to change your microbiome, I will still be wondering how much hype science is creating. 

I was having dinner with a non-scientitst, interested in science, the other night and they were reading loads of books on the gut and the microbiome, to the hype is being bought. Can it influence immunity? Probably, but is it a solution? I doubt it.

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  • Would the Appendix have any influence on this change in the gut microbiome?
    I had to take the appendix that suppurated when I was 16, shortly after an intense swim training.

    I only know that when I take probiotics my gut works better …

  • My gut has been in deep trouble for awhile, confounding my gastroenterologist and causing MS exacerbations. What's the solution? Probiotics? Done. Cranberry? Done. Eating a bland diet? Done. Drinking tons of purified water? Done. Onto a bacteria test in January. I've been reading and listening to lectures about the gut microbiome and MS and I'd love to have answers. Soon. My gut and my MS are sick and tired of being sick and tired.

  • Dr, let's say that self-intolerance was caused by exposure to the EBV antigen. Applying this logic, immunizing me against EBV wouldn't affect this aberrant immune response. While I don't believe that the microbiome causes MS or influences it (I believe my gut problems are due to things moving slowly, because of you know, nerve damage), I don't really follow the logic that correcting the microbiome in the susceptible would correlate to an improvement or reversal of symptomatic EAE.

  • I'm actually participating in a study right now. At this stage, I am giving blood. About 50% of us, w over represented progressive MSers, seemingly those w active disease, are low in a certain bacterial excrement lipid. The doc's MS mice were also low in this lipid and he was able to largely cure disease in the mice via supplementation of the lipid. He expects human trials in 1 1/2 yrs. Certainly hoping he's onto something, especially as I'm in the high match group.

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