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    Home > Active Ingredient News > Immunology News > Science: Your rheumatoid arthritis may be related to gut bacteria!

    Science: Your rheumatoid arthritis may be related to gut bacteria!

    • Last Update: 2023-01-06
    • Source: Internet
    • Author: User
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    , this is something I didn't expect.
    .
    .
    .




    Executive Summary


    A study published October 26 in Science Translational Medicine showed that a unique bacterium found in the gut can trigger rheumatoid arthritis (RA).


    Study screenshots

    status quo


    The mucosal origin hypothesis of RA points to the important role
    of mucosal immune responses in the initiation and continuation of systemic autoimmunity.
    However, the exact link between the RA mucosa and systemic autoimmunity remains unclear
    .
    Lead author Dr.
    Kristine Kuhn, Associate Professor of Rheumatology at the University of Colorado School of Medicine, said:

    • We can identify people at risk of RA based on serological markers, and these markers can be present in the blood for many years before diagnosis;
    • When these antibodies are observed, in addition to the normal class of antibodies, we can find antibodies associated with the mucosa, including the oral mucosa, intestinal mucosa, and lung mucosa
      .
      We began to suspect that there were substances
      within the mucosal barrier involved in driving RA.

    conclusion


    The research team conducted a series of in vitro experiments and animal model experiments using immunoglobulin A (IgA) and IgG family plasmablast-derived monoclonal autoantibodies obtained from the peripheral blood of individuals at high risk of RA and found:
    • After mixing the antibodies produced by individual immune cells at risk of RA with the feces of high-risk individuals, antibody-labeled bacteria can be found in the stool, and cross-reactivity between autoantigens associated with RA and bacterial taxa of Lachnospiraceae and Ruminococcaceae was identified.

    • Isolation of bacterial isolates of Lachnospiraceae/Ruminococcaceae subdoligranulum from individual feces confirmed that monoclonal antibody binding and CD4+ T cell activation in RA individuals compared to control individuals meant that T cells in the blood of RA patients responded to these bacteria, but otherwise healthy people did not;
    • Introduction of Subdoligranulum isolate into mice can lead to the development of blood markers associated with RA risk, and some of these animal models show the development of comprehensive RA;
    • These results suggest that specific gut bacteria can drive systemic autoantibody production and joint-centric antibody deposition and immune activation
      .

    prospect


    This study identified gut bacteria associated with RA risk through human trials and animal model experiments that trigger RA-like diseases in animal models, triggering RA-specific immune responses
    in humans.

    Kuhn said:
    • The unique species of bacteria that drive the immune response leads to RA in individuals who are already at risk, which means that we have discovered a new target for RA that can be targeted with drugs in the future to prevent this response from occurring;
    • In the next study, we will determine whether these bacteria are associated with other genetic, environmental, and mucosal immune responses in individuals at risk of RA, and ultimately identify them as a marker that can help predict the occurrence of RA;
    • It has long been thought that antibiotics may be a useful treatment for RA, a traditional antibiotic that will destroy a large number of bacteria; Our research may help to circumvent the sledgehammer effect of traditional antibiotics and selectively target a certain bacterium or its effects;
    • Many different technologies for selectively targeting the gut microbiome are emerging, and we will continue to study the mechanisms by which these bacteria trigger immune responses to ultimately block the pathogenic ability of these bacteria and explore prevention strategies to ultimately treat RA
      .


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