Activation of the complement cascade by Bordetella pertussis.
Bordetella pertussis must survive the defenses of the human respiratory tract including the complement system. The BrkA (Bordetella resistance to killing) protein prevents killing by the antibody-dependent classical pathway. In this study, the ability of B. pertussis to activate the human complement cascade by other pathways was examined. B. pertussis was not killed in serum depleted of C2, however serum depleted for factor B killed B. pertussis as efficiently as intact serum, suggesting complement activation occurred exclusively by the classical pathway. B. pertussis was not killed by serum depleted of antibody, suggesting the bacteria fail to activate the antibody-independent branches of the classical pathway, including the mannose binding lectin pathway. Mutants lacking the terminal trisaccharide of lipopolysaccharide retained the complement-resistant phenotype, suggesting this structure does not influence activation of complement.
Barnes
Michael G
MG
Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, 231 Sabin Way, ML 0524, Cincinnati, OH 45267, USA.
Weiss
Alison A
AA
D001886:Bordetella pertussis / Q000254:growth & development / Q000472:pathogenicity*; D015922:Complement C1q / Q000276:immunology; D003171:Complement Pathway, Classical; D003165:Complement System Proteins / Q000378:metabolism / Q000633:toxicity; D007113:Immunity, Innate; D008070:Lipopolysaccharides / Q000378:metabolism; D037601:Mannose-Binding Lectin / Q000378:metabolism; D008954:Models, Biological; D009154:Mutation; D014917:Whooping Cough / Q000097:blood / Q000276:immunology
D008070:Lipopolysaccharides; D037601:Mannose-Binding Lectin; D015922:Complement C1q; D003165:Complement System Proteins