Monday, October 31, 2011

microbiota greenlights brain inflammation

For the past few years published literature in immunology became enriched in studies related to commensial microbiota found mainly in mammalian gut. There is one simple explanation for this renewed interest in commensial microbiota: discovery and characterization of Toll-like receptors (TLRs) in late 90's (recognized by Nobel prize in Physiology or Medicine 2011). TLRs opened the door to study microbiota-host interaction at molecular level and made it easy to explain experimental observations mechanistically. In general, commensial microbiota could influence immune system in two ways: first, it could provide the antigenic material for adaptive immune system activation (T or B cells activation) and second, it could provide TLR ligands for innate immune system activation.

If you are interested to know more about commensial microbiota-host interaction, I will recommend to read the following article recently published in Nature. This study by Kerstin Berer et al. (1), examined the effect of commensial microbiota on the development of brain autoimmune disease in SJL/J TCR transgenic mice. In this mouse, if housed in a regular laboratory mouse facility, brain inflammation occurs spontaneously and is mediated by combined effect of MOG-specific T cells and B cells. However, according to this study, this type of brain inflammation does not occur in this mouse made germ-free (in sterile, microbiota free state). The disease development in this mouse require the presence of MOG protein because in its absence there is no brain inflammation irrespective of presence of absence of commensial microbiota. This results suggest that microbiota provide antigen-independent effect leading to stimulation of MOG-specifc T and B cells. However, how microbiota does it is not clear. The authors showed that there is reduction of IL-17 producing T cells in the gut of germ-free mouse. However, the authors provide no direct evidence whether IL-17-producing T cells play any role in disease development.

David Usharauli                  

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