• A normally harmless bacterium that can cause an IBD-like disease in tests

    Enterococcus faecalis is a commensal bacterium that is normally resident in the human gut, but like many such organisms it can cause harm in certain circumstances. The family to which this bacterium belongs has been noted to be increased in some subjects with IBD, and imbalances of normally harmless, but potentially pro-inflammatory organisms such as E. faecalis are thought important in the development of IBD.

    This paper from researchers in Germany, USA and Ireland focuses on E. faecalis, one of its enzymes and their relationship to an IBD-like change in mice known to be prone to an IBD-like disease. 60% of E. faecalis strains produce a powerful protein-digesting enzyme called gelatinase. This can result in damage to important structures of the gut in healthy hosts which act as barriers against invading bacteria. The researchers used E. faecalis strains both with and without the ability to produce this enzyme and introduced them to mice with impaired immune systems and no other gut bacteria (“germ-free” mice) to determine how much IBD-like inflammatory change was produced. Intestinal inflammation was most apparent in germ-free mice exposed to E. faecalis with the ability to produce gelatinase. Germ-free mice exposed to strains unable to produce this enzyme had a mild degree of inflammation only. Interestingly, when E. faecalis was given to mice with normal gut bacteria (“wild-type” mice), no inflammatory response was seen.

    This study shows that in the correct conditions (in this case mice with an impaired immune system and no gut bacteria) that E. faecalis can cause inflammatory change but that this is intensified if it is able to produce a specific enzyme and hence disrupt the normal barriers of the gut. If any of these 4 steps were altered (mouse immunity, mouse gut bacteria, E. faecalis, ability to produce enzyme) the inflammation either did not occur or was less intense. In humans a similar set of circumstances may be necessary for the development of IBD; however our knowledge of the required steps is limited. Studies such as this in a simplified mouse model of IBD allow the exploration of single steps, one-at-a-time, which can inform and improve our understanding of human IBD.

    RH

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