Wilden Janine J, Hrincius Eike R, Niemann Silke, Boergeling Yvonne, Löffler Bettina, Ludwig Stephan, Ehrhardt Christina
Institute of Virology Muenster (IVM), Westfaelische Wilhelms-University Muenster, 48149 Muenster, Germany.
Institute of Medical Microbiology, Westfaelische Wilhelms-University Muenster, 48149 Muenster, Germany.
Microorganisms. 2020 Dec 15;8(12):1998. doi: 10.3390/microorganisms8121998.
Human beings are exposed to microorganisms every day. Among those, diverse commensals and potential pathogens including () compose a significant part of the respiratory tract microbiota. Remarkably, bacterial colonization is supposed to affect the outcome of viral respiratory tract infections, including those caused by influenza viruses (IV). Since 30% of the world's population is already colonized with that can develop metabolically inactive dormant phenotypes and seasonal IV circulate every year, super-infections are likely to occur. Although IV and super-infections are widely described in the literature, the interactions of these pathogens with each other and the host cell are only scarcely understood. Especially, the effect of quasi-dormant bacterial subpopulations on IV infections is barely investigated. In the present study, we aimed to investigate the impact of small colony variants on the cell intrinsic immune response during a subsequent IV infection in vitro. In fact, we observed a significant impact on the regulation of pro-inflammatory factors, contributing to a synergistic effect on cell intrinsic innate immune response and induction of harmful cell death. Interestingly, the cytopathic effect, which was observed in presence of both pathogens, was not due to an increased pathogen load.
人类每天都暴露于微生物之中。其中,包括()在内的各种共生菌和潜在病原体构成了呼吸道微生物群的重要组成部分。值得注意的是,细菌定植被认为会影响病毒性呼吸道感染的结果,包括由流感病毒(IV)引起的感染。由于全球30%的人口已经被能够形成代谢不活跃休眠表型的()定植,且季节性流感病毒每年都会传播,因此很可能会发生重叠感染。尽管流感病毒和()重叠感染在文献中已有广泛描述,但这些病原体之间以及与宿主细胞的相互作用却鲜为人知。特别是,准休眠细菌亚群对流感病毒感染的影响几乎未被研究。在本研究中,我们旨在调查()小菌落变体对体外后续流感病毒感染期间细胞固有免疫反应的影响。事实上,我们观察到其对促炎因子调节有显著影响,这有助于对细胞固有先天免疫反应产生协同作用并诱导有害的细胞死亡。有趣的是,在两种病原体同时存在的情况下观察到的细胞病变效应并非由于病原体载量增加。