Pathogenesis ofCampylobacter fetusInfections: Critical Role of High-Molecular- Weight S-Layer Proteins in Virulence

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Abstract
Wild-type Campylobacter fetus strains possess high-molecular-weight S-Iayer proteins (S+) and are highly resistant to serum-mediated killing and phagocytosis. Spontaneous mutant strains lacking these proteins (S−) are serum and phagocytosis sensitive and have reduced virulence in a mouse model. Intact S+ cells were treated with pronase, which made them S− although genotypically S+ and had essentially no effect on other cellular proteins or on viability. Treatment with pronase, but not buffer alone, rendered these cells serum and phagocytosis sensitive and reduced mouse virulence to the level observed for the S− mutant cells. In related studies, purified S-Iayer proteins diminished neutrophil chemoluminescent responses to a heterologous particulate antigen. Finally, passive administration of antiserum to the 97-kDa S-Iayer protein partially protected mice against lethal challenge with the S+ strain. These studies define the contribution of the S-Iayer proteins to C. fetus virulence.

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