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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Signals involved in biofilm formation are often studied from a mechanistic perspective, which emphasizes their population-level effects. By adopting an informational perspective of signaling, we highlight the overlooked possibility that secreted factors which coordinate biofilm formation and facilitate interspecies competition, may also facilitate competition within the biofilm. We would like to acknowledge the late Prof. Amotz Zahavi, an inspiring mentor who imparted numerous thought-provoking discussions bridging zoology, ecology and microbiology in this Environmental Microbiology mini review.