The 12th Invest in ME Research Conference June, 2017, Part 2
MEMum presents the second article in a series of three about the recent 12th Invest In ME International Conference (IIMEC12) in London.
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Probiotics Signal Host Immune Cells

Discussion in 'Latest ME/CFS Research' started by kolowesi, Sep 24, 2009.

  1. kolowesi

    kolowesi Senior Member

    Central Texas
    This is from the latest Swanson newsletter:

    Lee Swanson Research Update
    Could Probiotics Protect Us From Gut Parasites?
    September 2009

    The gut-health benefits of probiotics may also extend to preventing and eradicating parasitic infections, according to early data from researchers at the University of Texas Southwestern.

    Scientists studying Toxoplasma gondii, the parasite responsible for toxoplasmosis, found that bacteria present in the human gut help stimulate the body's defense mechanisms.

    "While this is very early data, our results suggest that looking at the bacteria present in each patient's gut could help physicians understand their susceptibility to infectious diseases," said Dr. Felix Yarovinski from the University of Texas Southwestern. "It also suggests the possibility of developing novel probiotic strategies for treating parasitic infections such as toxoplasmosis and cryptosporidiosis, a related disease caused by the parasite Cryptosporidum."

    The UT Southwestern researchers published their findings in Cell Host & Microbe.

    Dr. Yarovinsky said that probiotics may occupy space in the intestine and thus reduce or prevent potentially pathogenic bacteria attaching to the intestinal wall.

    "In our work we revealed a novel feature of the beneficial relationship between commensal microorganisms and the host immune system," he said. "We found that gut commensal bacteria function as a molecular adjuvant, providing toll-like receptor (TLR)-dependent immunostimulatory signals to dendritic cells, which are the active mechanism of defense."

    The researchers used mice that had an inactivated form of a specific immune protein, called toll-like receptor 11 (TLR-11), which plays a role in controlling the animals' immune response to the parasite. While TLR-11 is normally active in mice, humans do not have an active form of the receptor. It has therefore remained unclear quite how the human body "senses" T gondii.

    Despite a lack of normal defense mechanisms, the researchers noted that the animals immune systems did react to T gondii infection.

    The researchers found that the commensalor goodbacteria in the gut activated the immune systems, thereby inducing various inflammatory responses against the invading pathogen. "This seems to be the first example of direct pathogen recognition in vivo where activation of the immune system depends on indirect rather than direct sensing of a pathogen," said Dr. Yarovinsky.

    And the potential benefits of the gut microflora appear to outweigh the benefits of having a full-functioning TLR-11, said Dr. Yarovinsky. In mice the receptor appears to do more harm than good.

    TLR-11-deficient mice were able to mobilize enough signaling proteins, with the help of their commensal bacteria, to defeat the parasite, while mice with the receptor activated too many signaling proteins and developed severe inflammation in their small intestines.

    Cell Host & Microbe 6(2):187-196, 2009

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