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Researchers investigated how gut bacteria persist under salt stress by studying a defined bacterial consortium in the intestine. They found that as intestinal salt concentration increases, a bacterium's ability to grow in laboratory conditions becomes more predictive of its abundance in the gut. However, in Bacteroides thetaiotaomicron, survival was higher than growth rate alone could explain, and they discovered that reduced cell death—achieved through rapid, reversible switching of surface proteins rather than genetic mutations—played a critical role in persistence under prolonged salt stress.
Why it matters
This research reveals that microbial survival in the gut depends not only on growth rate but also on minimizing cell death, providing new insights into how beneficial gut bacteria maintain their populations during environmental stress. Understanding these mechanisms could inform strategies for promoting beneficial microbiome composition in conditions where gut salt levels are elevated, such as high-salt diets or certain digestive disorders.
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⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
Microbial persistence in the gut is central to sustaining beneficial host-microbiota interactions; however, characterizing determinants of persistence in vivo can be challenging due to the complexity of native microbial communities interacting with the host. Here, we used a defined microbial consortium to demonstrate that intrinsic in vitro growth capacity becomes increasingly predictive of in vivo relative abundance as intestinal osmolality increases. In Bacteroides thetaiotaomicron, in vivo abundance was higher than predicted from growth capacity alone, indicating that additional physiological factors contribute to persistence. We identify mortality as one such determinant: adaptation to prolonged osmotic stress markedly reduced cell loss without enhancing growth capacity. This adaptive phenotype was associated with rapid and reversible phase variation in cell surface-associated PUL78/80 rather than fixed de novo mutations, with the PUL78/80-OFF state becoming progressively enriched among surviving cells as mortality increased. Our findings demonstrate that in addition to growth capacity, reduced cell loss can provide a distinct route to microbial persistence during environmental perturbation.