The microbiota shields the host against infections in a process known as colonization resistance. How infections themselves shape this fundamental process remains largely unknown. Here, we show that gut microbiota from previously infected hosts display enhanced resistance to infection. This long-term functional remodeling is associated with altered bile acid metabolism leading to the expansion of taxa that utilize the sulfonic acid taurine. Notably, supplying exogenous taurine alone is sufficient to induce this alteration in microbiota function and enhance resistance. Mechanistically, taurine potentiates the microbiota’s production of sulfide, an inhibitor of cellular respiration, which is key to host invasion by numerous pathogens. As such, pharmaceutical sequestration of sulfide perturbs the microbiota’s composition and promotes pathogen invasion. Together, this work reveals a process by which the host, triggered by infection, can deploy taurine as a nutrient to nourish and train the microbiota, promoting its resistance to subsequent infection.

微生物群在称为定植抵抗的过程中保护宿主免受感染。感染本身如何塑造这一基本过程仍然很大程度上未知。在这里，我们发现来自先前感染宿主的肠道微生物群表现出增强的感染抵抗力。这种长期的功能重塑与胆汁酸代谢的改变有关，导致利用磺酸牛磺酸的类群扩张。值得注意的是，仅提供外源牛磺酸就足以诱导微生物群功能的这种改变并增强抵抗力。从机制上讲，牛磺酸可增强微生物群产生硫化物，硫化物是细胞呼吸的抑制剂，是许多病原体入侵宿主的关键。因此，硫化物的药物封存会扰乱微生物群的组成并促进病原体入侵。总之，这项工作揭示了一个过程，在这个过程中，感染引发的宿主可以利用牛磺酸作为营养物质来滋养和训练微生物群，从而促进其对后续感染的抵抗力。