CAS & Shandong Province Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao, 266071, China.
Tianjin Key Laboratory of Animal and Plant Resistance, College of Life Sciences, Tianjin Normal University, 393 West Binshui Road, Xiqing District, Tianjin, 300387, China.
Commun Biol. 2022 Jun 29;5(1):637. doi: 10.1038/s42003-022-03587-3.
Edwardsiella tarda is a well-known bacterial pathogen with a broad range of host, including fish, amphibians, and mammals. One eminent virulence feature of E. tarda is its strong ability to resist the killing of host serum complement, but the involving mechanism is unclear. In this report, we identified E. tarda TraT as a key player in both complement resistance and cellular invasion. TraT, a surface-localized protein, bound and recruited complement factor H onto E. tarda, whereby inhibiting complement activation via the alternative pathway. TraT also interacted with host CD46 in a specific complement control protein domain-dependent manner, whereby facilitating the cellular infection and tissue dissemination of E. tarda. Thus, by acting as an anti-complement factor and a cellular infection promoter, TraT makes an important contribution to the complement evasion and systemic infection of E. tarda. These results add insights into the pathogen-host interaction mechanism during E. tarda infection.
迟缓爱德华氏菌是一种具有广泛宿主范围的著名细菌病原体，包括鱼类、两栖类和哺乳动物。迟缓爱德华氏菌的一个显著毒力特征是其强烈的抵抗宿主血清补体杀伤的能力，但涉及的机制尚不清楚。在本报告中，我们鉴定出迟缓爱德华氏菌 TraT 是补体抵抗和细胞入侵的关键因子。TraT 是一种表面定位的蛋白，将补体因子 H 结合并募集到迟缓爱德华氏菌上，从而通过替代途径抑制补体激活。TraT 还以特定的补体控制蛋白结构域依赖性方式与宿主 CD46 相互作用，从而促进迟缓爱德华氏菌的细胞感染和组织传播。因此，TraT 作为一种抗补体因子和细胞感染促进因子，对迟缓爱德华氏菌的补体逃避和全身感染做出了重要贡献。这些结果为迟缓爱德华氏菌感染过程中的病原体-宿主相互作用机制提供了新的见解。
