Immunobiology Department, University of Arizona, Tucson, Arizona, United States of America.
BIO5 Institute, University of Arizona, Tucson, Arizona, United States of America.
PLoS Pathog. 2022 May 17;18(5):e1010497. doi: 10.1371/journal.ppat.1010497. eCollection 2022 May.
The mechanisms used by human adapted commensal Neisseria to shape and maintain a niche in their host are poorly defined. These organisms are common members of the mucosal microbiota and share many putative host interaction factors with Neisseria meningitidis and Neisseria gonorrhoeae. Evaluating the role of these shared factors during host carriage may provide insight into bacterial mechanisms driving both commensalism and asymptomatic infection across the genus. We identified host interaction factors required for niche development and maintenance through in vivo screening of a transposon mutant library of Neisseria musculi, a commensal of wild-caught mice which persistently and asymptomatically colonizes the oral cavity and gut of CAST/EiJ and A/J mice. Approximately 500 candidate genes involved in long-term host interaction were identified. These included homologs of putative N. meningitidis and N. gonorrhoeae virulence factors which have been shown to modulate host interactions in vitro. Importantly, many candidate genes have no assigned function, illustrating how much remains to be learned about Neisseria persistence. Many genes of unknown function are conserved in human adapted Neisseria species; they are likely to provide a gateway for understanding the mechanisms allowing pathogenic and commensal Neisseria to establish and maintain a niche in their natural hosts. Validation of a subset of candidate genes confirmed a role for a polysaccharide capsule in N. musculi persistence but not colonization. Our findings highlight the potential utility of the Neisseria musculi-mouse model as a tool for studying the pathogenic Neisseria; our work represents a first step towards the identification of novel host interaction factors conserved across the genus.
人体共生奈瑟菌用于塑造和维持其宿主小生境的机制尚未完全明确。这些生物体是黏膜微生物群的常见成员,与脑膜炎奈瑟菌和淋病奈瑟菌具有许多假定的宿主相互作用因子。评估这些共享因子在宿主携带过程中的作用可能有助于深入了解驱动属内共生和无症状感染的细菌机制。我们通过对野生捕获小鼠共生菌肌肉奈瑟菌的转座子突变体文库进行体内筛选,确定了小生境发育和维持所需的宿主相互作用因子。大约鉴定出 500 个与长期宿主相互作用相关的候选基因。这些基因包括已被证明可在体外调节宿主相互作用的脑膜炎奈瑟菌和淋病奈瑟菌毒力因子的同源物。重要的是,许多候选基因没有指定的功能,这说明我们对奈瑟菌的持久性还有很多需要了解。许多未知功能的基因在适应人体的奈瑟菌物种中是保守的;它们可能为理解允许致病性和共生性奈瑟菌在其自然宿主中建立和维持小生境的机制提供一个切入点。对一组候选基因的验证证实了多糖荚膜在肌肉奈瑟菌持久性中的作用,但对定植没有作用。我们的研究结果强调了肌肉奈瑟菌-小鼠模型作为研究致病性奈瑟菌的工具的潜力;我们的工作代表了确定属内保守的新型宿主相互作用因子的第一步。