PDF(Pubmed)
Abstract：
The mammalian gut microbiota is a complex community of microorganisms which typically exhibits remarkable stability. As the gut microbiota has been shown to affect many aspects of host health, the molecular keys to developing and maintaining a \"healthy\" gut microbiota are highly sought after. Yet, the qualities that define a microbiota as healthy remain elusive. We used the ability to resist change in response to antibiotic disruption, a quality we refer to as ecological resistance, as a metric for the health of the bacterial microbiota. Using a mouse model, we found that colonization with the commensal fungus Candida albicans decreased the ecological resistance of the bacterial microbiota in response to the antibiotic clindamycin such that increased microbiota disruption was observed in C. albicans-colonized mice compared to that in uncolonized mice. C. albicans colonization resulted in decreased alpha diversity and small changes in abundance of bacterial genera prior to clindamycin challenge. Strikingly, co-occurrence network analysis demonstrated that C. albicans colonization resulted in sweeping changes to the co-occurrence network structure, including decreased modularity and centrality and increased density. Thus, C. albicans colonization resulted in changes to the bacterial microbiota community and reduced its ecological resistance.IMPORTANCECandida albicans is the most common fungal member of the human gut microbiota, yet its ability to interact with and affect the bacterial gut microbiota is largely uncharacterized. Previous reports showed limited changes in microbiota composition as defined by bacterial species abundance as a consequence of C. albicans colonization. We also observed only a few bacterial genera that were significantly altered in abundance in C. albicans-colonized mice; however, C. albicans colonization significantly changed the structure of the bacterial microbiota co-occurrence network. Additionally, C. albicans colonization changed the response of the bacterial microbiota ecosystem to a clinically relevant perturbation, challenge with the antibiotic clindamycin.
摘要：
哺乳动物肠道微生物群是复杂的微生物群落,其通常表现出显著的稳定性。由于肠道微生物群已经被证明会影响宿主健康的许多方面，开发和维持“健康”肠道微生物群的分子关键备受追捧。然而，将微生物群定义为健康的品质仍然难以捉摸。我们利用了抵抗抗生素破坏的变化的能力，我们称之为生态抗性的品质，作为衡量细菌微生物群健康的指标。使用鼠标模型，我们发现共生真菌白色念珠菌的定植降低了细菌微生物群对抗生素克林霉素的生态抗性，因此与未定植小鼠相比，白色念珠菌定植小鼠的微生物群破坏增加。白色念珠菌定植导致在克林霉素攻击之前α多样性降低和细菌属丰度的小变化。引人注目的是，共现网络分析表明，白色念珠菌定植导致共现网络结构发生了巨大变化，包括降低的模块性和中心性以及增加的密度。因此，白色念珠菌定植导致细菌微生物群落的变化并降低其生态抗性。重要性白色念珠菌是人类肠道菌群中最常见的真菌成员，然而，它与细菌肠道微生物群相互作用并影响细菌肠道微生物群的能力在很大程度上是未知的。以前的报告显示，由于白色念珠菌定殖，由细菌物种丰度定义的微生物群组成变化有限。我们还观察到只有少数细菌属在白色念珠菌定植的小鼠中丰度显著改变；然而，白色念珠菌定植显著改变了细菌微生物群共生网络的结构。此外,白色念珠菌定植改变了细菌微生物群生态系统对临床相关扰动的反应，用抗生素克林霉素挑战。
