Abstract
AbstractEdwardsiella tardais a well-known bacterial pathogen with a broad range of host, including fish, amphibians, and mammals. One eminent virulence feature ofE. tardais its strong ability to resist the killing of host serum complement, but the involving mechanism is unclear. In this report, we identifiedE. tardaTraT as a key player in both complement resistance and cellular invasion. TraT, a surface-localized protein, bound and recruited complement factor H ontoE. 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 ofE. 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 ofE. tarda. These results add insights into the pathogen-host interaction mechanism duringE. tardainfection.
Funder
the National Key Research and Development Program of China, and the Taishan Scholar Program of Shandong Province.
Publisher
Springer Science and Business Media LLC
Subject
General Agricultural and Biological Sciences,General Biochemistry, Genetics and Molecular Biology,Medicine (miscellaneous)
Cited by
15 articles.
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