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Bacterial Changes may trigger diseases like Rheumatoid Arthritis

Discussion in 'Other Health News and Research' started by Glynis Steele, Jun 12, 2012.

  1. Glynis Steele

    Glynis Steele Senior Member

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    Newcastle upon Tyne UK
    ScienceDaily (June 11, 2012) — The billions of bugs in our guts have a newfound role: regulating the immune system and related autoimmune diseases such as rheumatoid arthritis, according to researchers at Mayo Clinic and the University of Illinois at Urbana-Champaign.

    Larger-than-normal populations of specific gut bacteria may trigger the development of diseases like rheumatoid arthritis and possibly fuel disease progression in people genetically predisposed to this crippling and confounding condition, say the researchers, who are participating in the Mayo Illinois Alliance for Technology Based Healthcare.

    The study is published in the April 2012 issue of PLoS ONE. "A lot of people suspected that gut flora played a role in rheumatoid arthritis, but no one had been able to prove it because they couldn't say which came first -- the bacteria or the genes," says senior author Veena Taneja, Ph.D., a Mayo Clinic immunologist. "Using genomic sequencing technologies, we have been able to show the gut microbiome may be used as a biomarker for predisposition."

    Researchers found that hormones and changes related to aging may further modulate the gut immune system and exacerbate inflammatory conditions in genetically susceptible individuals.
    Nearly 1 percent of the world's population has rheumatoid arthritis, a disease in which the immune system attacks tissues, inflaming joints and sometimes leading to deadly complications such as heart disease. Other diseases with suspected gut bacterial ties include type I diabetes and multiple sclerosis.
    Full article here: http://www.sciencedaily.com/releases/2012/06/120611193342.htm
     
  2. Enid

    Enid Senior Member

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    Interesting Glynis thanks - good to see GI function receiving so much attention at last.
     
  3. Waverunner

    Waverunner Senior Member

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    Thanks for posting it, Glynis. Here we go again, all the studies come to the same conclusion: Stop translocation of bacteria! It's time that science and doctors pick up on this.
    From the above source: http://www.sciencedaily.com/releases/2012/06/120611193342.htm
    ...​
    "The gut is the largest immune organ in the body," says co-author Bryan White, Ph.D., director of the University of Illinois' Microbiome Program in the Division of Biomedical Sciences and a member of the Institute for Genomic Biology. "Because it's presented with multiple insults daily through the introduction of new bacteria, food sources and foreign antigens, the gut is continually teasing out what's good and bad."
    The gut has several ways to do this, including the mucosal barrier that prevents organisms -- even commensal or "good" bacteria -- from crossing the lumen of the gut into the human body. However, when commensal bacteria breach this barrier, they can trigger autoimmune responses. The body recognizes them as out of place, and in some way this triggers the body to attack itself, he says."...
     
  4. pattismith

    pattismith Senior Member

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    The two articles published in 2016 by Veena and col from Mayo are very important ones!
    Our condition may have similar origin as well...(maybe not the same bacteria involved thoguh)


    "RESULTS:
    Patients with RA exhibited decreased gut microbial diversity compared with controls, which correlated with disease duration and autoantibody levels. A taxon-level analysis suggested an expansion of rare taxa, Actinobacteria, with a decrease in abundant taxa in patients with RA compared with controls. Prediction models based on the random forests algorithm suggested that three genera, Collinsella, Eggerthella, and Faecalibacterium, segregated with RA. The abundance of Collinsella correlated strongly with high levels of alpha-aminoadipic acid and asparagine as well as production of the proinflammatory cytokine IL-17A. A role for Collinsella in altering gut permeability and disease severity was confirmed in experimental arthritis.

    CONCLUSIONS:
    These observations suggest dysbiosis in RA patients resulting from the abundance of certain rare bacterial lineages. A correlation between the intestinal microbiota and metabolic signatures could determine a predictive profile for disease causation and progression."

    https://www.ncbi.nlm.nih.gov/pubmed/27102666

    and


    RESULTS:
    When treated with P histicola in prophylactic or therapeutic protocols, DQ8 mice exhibited significantly decreased incidence and severity of arthritis compared to controls. The microbial mucosal modulation of arthritis was dependent on regulation by CD103+ dendritic cells and myeloid suppressors (CD11b+Gr-1+ cells) and by generation of Treg cells (CD4+CD25+FoxP3+) in the gut, resulting in suppression of antigen-specific Th17 responses and increased transcription of interleukin-10. Treatment with P histicola led to reduced intestinal permeability by increasing expression of enzymes that produce antimicrobial peptides as well as tight junction proteins (zonula occludens 1 and occludin). However, the innate immune response via Toll-like receptor 4 (TLR-4) and TLR-9 was not affected in treated mice.

    CONCLUSION:
    Our results demonstrate that enteral exposure to Prevotella Histicola suppresses arthritis via mucosal regulation. P histicola is a unique commensal that can be explored as a novel therapy for RA and may have few or no side effects.

    https://www.ncbi.nlm.nih.gov/pubmed/27337150
     
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  5. pattismith

    pattismith Senior Member

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    Prevotella H could be also effective on MS, the bacteria colonize the upper digestive tract:


    Treatment with P. histicola Reduced Inflammation and Demyelination in the CNS
    Analysis of CNS tissues from medium-challenged HLA-DR3.DQ8 transgenic mice showed severe inflammation and demyelination in the brain and spinal cord compared to the P. histicola-challenged groups (Figure 1C). Quantitative analysis of spinal cord inflammation and demyelination showed that P. histicola-challenged animals had fewer regions with inflammation and demyelination (Figure 1D). Groups receiving other bacteria (E. coli and C. sputigena) had severe CNS inflammation and demyelination, similar to the medium-challenged group. Thus, treatment with P. histicola reduced CNS inflammation and demyelination, compared to the medium-only group.

    http://www.cell.com/cell-reports/fu...m/retrieve/pii/S221112471730997X?showall=true
     
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