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Gut colonization by oral bacteria, especially Klebsiella species, had been responsible for a T-helper 1 (TH1) cell induction and inflammation in genetically susceptible host [46]

hidden platform), it may be a difference in strategy, rather than in learning or memory, that dominates the response of knockout, compared to wild-type, mice

Braz J Plant Physiol

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Molecular mechanism of nrf2 activation by oxidative stress

One hypothesis for RA pathogenesis is that the disease begins in genetically predisposed individuals at mucosal sites (i.e., oral cavity, lung, gut) as a consequence of the interaction between a dysbiotic microbiota and the mucosal immune system, and then transitions to synovitis [8]