Salmonella enterica serovar Typhimurium utilizes a series of strategies to evade host innate immune defenses, including the serum complement system. Many microbial pathogens have evolved the ability to bind the complement regulatory protein factor H (FH) through their surface factor H-binding proteins (FHBPs) to circumvent the complement-mediated bactericidal effect. However, the roles of FHBPs in Salmonella pathogenesis are not well understood. In this study, we demonstrated that the survival of S. Typhimurium in human serum was decreased in a time and concentration dependent manner. Pre-incubation with FH attenuated the sensitivity of S. Typhimurium strain χ3761 to complement-mediated serum killing, suggesting FH binding enhance survival in serum. We aimed to identify novel S. Typhimurium FHBPs and characterize their biological functions. Here, six potential FHBPs were identified by two-dimensional (2D)-Far-western blot, and three of them were further confirmed to bind FH by Far-western blot and dot blot. We found that deletion of ompC (ΔompC) significantly inhibited the survival of S. Typhimurium strain χ3761 in human serum. Our results indicated that the ompC mutation does not affect χ3761 adhesion to HeLa cells. Furthermore, a mice infection model showed that deletion of ompC had no significant effect on the histopathological lesions or viability compared with the wild-type strain χ3761. In summary, these results suggested that OmpC is an important FHBP, but not a critical virulence factor of S. Typhimurium.

肠沙门氏菌鼠伤寒血清型利用一系列策略来逃避宿主先天免疫防御，包括血清补体系统。许多微生物病原体已经进化出通过其表面 H 因子结合蛋白 (FHBP) 结合补体调节蛋白 H 因子 (FH) 的能力，从而规避补体介导的杀菌作用。然而，FHBP 在沙门氏菌发病机制中的作用尚不清楚。在这项研究中，我们证明了人血清中鼠伤寒沙门氏菌的存活率以时间和浓度依赖性方式降低。与 FH 预孵育减弱了鼠伤寒沙门氏菌菌株 χ3761 对补体介导的血清杀伤的敏感性，表明 FH 结合增强了血清中的存活率。我们的目的是鉴定新型鼠伤寒沙门氏菌 FHBP 并表征其生物学功能。在此，通过二维（2D）-Far-western blot鉴定了6种潜在的FHBP，其中3种通过Far-western blot和斑点印迹进一步证实与FH结合。我们发现ompC (Δ ompC ) 的缺失显着抑制了人血清中鼠伤寒沙门氏菌菌株χ3761 的存活。我们的结果表明ompC突变不影响 χ3761 对 HeLa 细胞的粘附。此外，小鼠感染模型表明，与野生型菌株χ3761相比， ompC的缺失对组织病理学病变或活力没有显着影响。总之，这些结果表明OmpC是一种重要的FHBP，但不是鼠伤寒沙门氏菌的关键毒力因子。