한빛사논문
Hwan Keun Kima,b,1, Ranjan Premaratnac, Dominique M. Missiakasa,b, and Olaf Schneewinda,b
a Howard Taylor Ricketts Laboratory, Argonne National Laboratory, Lemont, IL 60649; b Department of Microbiology, University of Chicago, Chicago, IL 60637; and c Department of Medicine, Faculty of Medicine, University of Kelaniya, Ragama 11010, Sri Lanka
1To whom correspondence may be addressed.
Abstract
Rickettsial diseases have long been diagnosed with serum antibodies cross-reactive against Proteus vulgaris (Weil–Felix reaction). Although Weil–Felix antibodies are associated with the development of immunity, their rickettsial target and contribution to disease pathogenesis are not established. Here, we developed a transposon for insertional mutagenesis of Rickettsia conorii, isolating variants defective for replication in cultured cells and in spotted fever pathogenesis. Mutations in the polysaccharide synthesis operon (pso) abolish lipopolysaccharide O-antigen synthesis and Weil–Felix serology and alter outer-membrane protein assembly. Unlike wild-type R. conorii, pso mutants cannot elicit bactericidal antibodies that bind O antigen. The pso operon is conserved among rickettsial pathogens, suggesting that bactericidal antibodies targeting O antigen may generate universal immunity that could be exploited to develop vaccines against rickettsial diseases.
transposon mutagenesis, lipopolysaccharide, O antigen, Weil–Felix reaction, polysaccharide synthesis operon
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