A balanced gut microbiota contributes to health, but the mechanisms maintaining homeostasis remain elusive. Microbiota assembly during infancy is governed by competition between species and by environmental factors, termed habitat filters, that determine the range of successful traits within the microbial community. These habitat filters include the diet, host-derived resources, and microbiota-derived metabolites, such as short-chain fatty acids. Once the microbiota has matured, competition and habitat filtering prevent engraftment of new microbes, thereby providing protection against opportunistic infections. Competition with endogenous Enterobacterales, habitat filtering by short-chain fatty acids, and a host-derived habitat filter, epithelial hypoxia, also contribute to colonization resistance against Salmonella serovars. However, at a high challenge dose, these frank pathogens can overcome colonization resistance by using their virulence factors to trigger intestinal inflammation. In turn, inflammation increases the luminal availability of host-derived resources, such as oxygen, nitrate, tetrathionate, and lactate, thereby creating a state of abnormal habitat filtering that enables the pathogen to overcome growth inhibition by short-chain fatty acids. Thus, studying the process of ecosystem invasion by Salmonella serovars clarifies that colonization resistance can become weakened by disrupting host-mediated habitat filtering. This insight is relevant for understanding how inflammation triggers dysbiosis linked to noncommunicable diseases, conditions in which endogenous Enterobacterales expand in the fecal microbiota using some of the same growth-limiting resources required by Salmonella serovars for ecosystem invasion. In essence, ecosystem invasion by Salmonella serovars suggests that homeostasis and dysbiosis simply represent states where competition and habitat filtering are normal or abnormal, respectively.

中文翻译：

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沙门氏菌与微生物组

平衡的肠道微生物群有助于健康，但维持体内平衡的机制仍然难以捉摸。婴儿期的微生物群组装受物种之间的竞争和环境因素（称为栖息地过滤器）的控制，这些因素决定了微生物群落内成功性状的范围。这些栖息地过滤器包括饮食、宿主来源的资源和微生物群来源的代谢物，如短链脂肪酸。一旦微生物群成熟，竞争和栖息地过滤会阻止新微生物的植入，从而防止机会性感染。与内源性肠杆菌的竞争、短链脂肪酸的栖息地过滤以及宿主衍生的栖息地过滤器、上皮缺氧，也有助于抗沙门氏菌血清型。然而，在高攻击剂量下，这些坦率的病原体可以通过使用其毒力因子触发肠道炎症来克服定植抵抗力。反过来，炎症会增加宿主来源资源的管腔可用性，例如氧气、硝酸盐、连四硫酸盐和乳酸盐，从而产生异常栖息地过滤状态，使病原体能够克服短链脂肪酸的生长抑制。因此，研究沙门氏菌血清型对生态系统的入侵过程表明，破坏宿主介导的栖息地过滤会削弱定植抵抗力。这一见解与理解炎症如何触发与非传染性疾病相关的生态失调有关，在这些疾病中，内源性肠杆菌利用沙门氏菌血清型入侵生态系统所需的一些相同的生长限制资源在粪便微生物群中扩张。从本质上讲，沙门氏菌血清型对生态系统的入侵表明，稳态和生态失调仅代表竞争和栖息地过滤分别正常或异常的状态。