Blötz Cedric, Singh Neil, Dumke Roger, Stülke Jörg
Department of General Microbiology, Göttingen Center for Molecular Biosciences, University of Göttingen, Göttingen, Germany.
Medical Faculty Carl Gustav Carus, Institute of Medical Microbiology and Hygiene, Technical University Dresden, Dresden, Germany.
Front Microbiol. 2020 Apr 16;11:685. doi: 10.3389/fmicb.2020.00685. eCollection 2020.
Bacteria evolved many ways to invade, colonize and survive in the host tissue. Such complex infection strategies of other bacteria are not present in the cell-wall less . Due to their strongly reduced genomes, these bacteria have only a minimal metabolism. is a pathogenic bacterium using its virulence repertoire very efficiently, infecting the human lung. can cause a variety of conditions including fever, inflammation, atypical pneumoniae, and even death. Due to its strongly reduced metabolism, is dependent on nutrients from the host and aims to persist as long as possible, resulting in chronic diseases. evolved strategies to subvert the host immune system which involve proteins fending off immunoglobulins (Igs). In this study, we investigated the role of MPN400 as the putative factor responsible for Ig-binding and host immune evasion. MPN400 is a cell-surface localized protein which binds strongly to human IgG, IgA, and IgM. We therefore named the protein MPN400 immunoglobulin binding protein of (IbpM). A strain devoid of IbpM is slightly compromised in cytotoxicity. Taken together, our study indicates that uses a refined mechanism for immune evasion.
细菌进化出多种方式在宿主组织中入侵、定殖和存活。其他细菌的这种复杂感染策略在无细胞壁细菌中并不存在。由于其基因组大幅缩减，这些细菌只有最低限度的代谢。[细菌名称]是一种致病性细菌，能非常有效地利用其毒力机制，感染人类肺部。[细菌名称]可引发多种病症，包括发热、炎症、非典型肺炎，甚至死亡。由于其代谢大幅降低，[细菌名称]依赖宿主的营养物质，并尽可能长期存活，从而导致慢性病。[细菌名称]进化出了颠覆宿主免疫系统的策略，其中涉及抵御免疫球蛋白（Igs）的蛋白质。在本研究中，我们调查了MPN400作为负责Ig结合和宿主免疫逃逸的假定因子的作用。MPN400是一种定位于细胞表面的蛋白质，它能与人类IgG、IgA和IgM强烈结合。因此，我们将该蛋白质命名为[细菌名称]的免疫球蛋白结合蛋白（IbpM）。缺失IbpM的菌株在细胞毒性方面略有受损。综上所述，我们的研究表明，[细菌名称]利用一种精细的机制进行免疫逃逸。
