In the current issue of Cell Host & Microbe, DePaolo and colleagues find that Yersinia enterocolitica infection of Tlr1−/− mice leads to elevated inflammatory signaling in the intestine months after the infection has resolved. This was likely due to the expansion of certain commensals such as Desulfovibrio desulfuricans or loss of others like several Lactobacilli species during Y. enterocolitica infection and the subsequent host immune response. Interestingly, when the altered microbiota was transferred into germ-free mice, they found that recipient mice became more sensitive to colitis and had similar elevated levels of the proinflammtory cytokines as the donor. Taken together, the authors suggests that even acute infections (and their long lasting perturbations on the microbiota) could serve as distant cues that can render people more susceptibility to later inflammatory events.
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