Open AccessThe Vi Capsular Polysaccharide Prevents Complement Receptor 3-Mediated Clearance of Salmonella enterica Serotype Typhi
Author(s) -
Ronald P. Wilson,
Sebastian Winter,
Alanna M. Spees,
Maria G. Winter,
Jessalyn H. Nishimori,
Juan Sánchez,
Sean Paul Nuccio,
Robert W. Crawford,
Çaǧla Tükel,
Andreas J. Bäumler
Publication year - 2011
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00961-10
Subject(s) - antibody opsonization , microbiology and biotechnology , biology , salmonella typhi , salmonella enterica , virulence , immune system , bacterial capsule , phagocytosis , innate immune system , complement system , antibody , serotype , classical complement pathway , salmonella , virology , bacteria , immunology , escherichia coli , opsonin , gene , biochemistry , genetics
Capsular polysaccharides are important virulence factors of invasive bacterial pathogens. Here we studied the role of the virulence (Vi) capsular polysaccharide ofSalmonella enterica serotype Typhi (S. Typhi) in preventing innate immune recognition by complement. Comparison of capsulatedS. Typhi with a noncapsulated mutant (ΔtviBCDE vexABCDE mutant) revealed that the Vi capsule interfered with complement component 3 (C3) deposition. Decreased complement fixation resulted in reduced bacterial binding to complement receptor 3 (CR3) on the surface of murine macrophagesin vitro and decreased CR3-dependent clearance of Vi capsulatedS. Typhi from the livers and spleens of mice. Opsonization of bacteria with immune serum prior to intraperitoneal infection increased clearance of capsulatedS. Typhi from the liver. Our data suggest that the Vi capsule prevents CR3-dependent clearance, which can be overcome in part by a specific antibody response.