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Effect of vaccine-elicited antibodies on colonization of Neisseria meningitidis serogroup B and C strains in a human bronchial epithelial cell culture model.

Capsular polysaccharide-protein conjugate vaccines protect individuals from invasive disease and decrease carriage, which reduces spread of the organism in the population. In contrast, antibodies elicited by plain polysaccharide or protein antigen-based meningococcal (Men) vaccines have little or no effect on decreasing carriage. In this study, we investigated the mechanism by which vaccine-induced human IgG antibodies affect colonization by serogroup B (MenB) or C (MenC) strains using a human bronchial epithelial cell culture model (16HBE14o-). Fluorescence microscopy showed bacteria colonizing the apical side of 16HBE14o- monolayers had decreased capsular polysaccharide on the bacterial surface that resulted from shedding the capsule and not decreased production of polysaccharide. Capsular polysaccharide shedding depended on the presence of 16HBE14o- cells and bacteria, but not direct adherence of the bacteria to the cells. Treatment of bacteria and cells with post immunization MenC-conjugate IgG or murine anti-MenB polysaccharide mAbs inhibited capsule shedding, microcolony dispersal, and invasion of the 16HBE14o- cell monolayer. In contrast, IgG elicited by immunization with MenC PS, MenB outer membrane vesicle (OMV)-, or Factor H binding protein (FHbp)-based vaccines were not different than pre-immune IgG or no treatment. The results provide new insights on the mechanism by which high avidity anticapsular antibodies elicited by polysaccharide-conjugate vaccines affect meningococcal colonization. The data also suggest that any effect on colonization by IgG elicited by OMV- or FHbp-based vaccines may involve a different mechanism.

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