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Abstract

Metabolic adaptation plays a key role in determining the composition of microbial ecosystems. A new study shows that in the inflamed gut, pathogenic Enterobacteriaceae can reprogramme their metabolism towards diet-derived l-serine utilization to outcompete the resident microbiota and cause disease.

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... In recent years, new and improved experimental approaches to study the gut-microbiota crosstalk have been developed. Because the gut microbiota profoundly influence the phenotype and function of the host immune system [22][23][24], most of the works have been focused on the interactions between the microbiota and the immune system of the host. Numerous population studies [25][26][27], germfree mice experiments [18,28,29], and in vitro platforms, e.g., gut on the chip [30], contributed to the accumulation of knowledge about these interactions. ...
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... In their recent "News and Views" article, Yoo and Byndloss (2020) highlighted the need to answer to the questions "who is there?" and "what are they doing?" about the microbial community during dysbiosis and intestinal inflammation. ...
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The bacterial microbiota of the human large bowel is a complex ecosystem consisting of several hundred, mostly anaerobic, species. To maintain colonization of the gut lumen and maximize growth in the presence of nutritional competitors, highly diverse metabolic pathways have evolved, with each microbe utilizing a different "winning strategy" for nutrient acquisition and utilization. Conditions and diseases leading to intestinal inflammation are accompanied by a severe disruption the microbiota composition characterized by an expansion of facultative anaerobic Enterobacteriaceae. Here, we review evidence that the local inflammatory response creates a unique nutritional environment that is conducive to a bloom of bacterial species whose genomes encode the capability of utilizing inflammation-derived nutrients.
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