Division of Integrated Biomedical Sciences, University of Detroit Mercy School of Dentistry, Detroit, MI, USA.
FEBS Lett. 2020 Aug;594(16):2598-2620. doi: 10.1002/1873-3468.13771. Epub 2020 Mar 30.
Pathogens that colonize deep tissues and spread systemically encounter the innate host resistance mechanism of complement-mediated lysis and complement opsonization leading to engulfment and degradation by phagocytic cells. Yersinia and Salmonella species have developed numerous strategies to block the antimicrobial effects of complement. These include recruitment of complement regulatory proteins factor H, C4BP, and vitronectin (Vn) as well as interference in late maturation events such as assembly of C9 into the membrane attack complex that leads to bacterial lysis. This review will discuss the contributions of various surface structures (proteins, lipopolysaccharide, and capsules) to evasion of complement-mediated immune clearance of the systemic pathogens Yersiniae and Salmonellae. Bacterial proteins required for recruitment of complement regulatory proteins will be described, including the details of their interaction with host regulatory proteins, where known. The potential role of the surface proteases Pla (Yersinia pestis) and PgtE (Salmonella species) on the activity of complement regulatory proteins will also be addressed. Finally, the implications of complement inactivation on host cell interactions and host cell targeting for type 3 secretion will be discussed.
定植于深部组织并播散全身的病原体，会遭遇补体介导的溶破和补体调理作用，从而被吞噬细胞吞噬和降解，这是宿主固有抵抗机制。耶尔森菌和沙门氏菌已开发出多种策略来阻断补体的抗菌作用。这些策略包括招募补体调节蛋白因子 H、C4BP 和 vitronectin（Vn），以及干扰 C9 装配到膜攻击复合物的晚期成熟事件，导致细菌裂解。这篇综述将讨论各种表面结构（蛋白质、脂多糖和荚膜）对逃避耶尔森氏菌和沙门氏菌系统病原体的补体介导免疫清除的作用。将描述招募补体调节蛋白所需的细菌蛋白，包括其与宿主调节蛋白相互作用的详细信息（如果已知的话）。表面蛋白酶 Pla（鼠疫耶尔森菌）和 PgtE（沙门氏菌属）对补体调节蛋白活性的潜在作用也将得到解决。最后，将讨论补体失活对宿主细胞相互作用和 III 型分泌的宿主细胞靶向的影响。
