Abstract
Abstract Secretory IgA (SIgA) antibodies directed against the O-antigen (O-Ag) component of lipopolysaccharide are the primary determinants of mucosal immunity to enteric bacterial pathogens, such as Shigella flexneri and Salmonella enteric serovar Typhimurium. In this report, we demonstrate that monoclonal IgA Abs against the O-Ag are effective inhibitors of the bacterial type 3 secretion systems (T3SS) required for bacterial entry into intestinal epithelial cells. While these Abs did not affect bacterial viability, they did transiently de-energize both S. flexneri and S. Typhimurium, possibly accounting for the “paralysis” that has been observed in the case of S. Typhimurium, following Ab treatment. O-Ag specific IgA Abs also elicited long lasting ultrastructural changes in the bacterial outer membranes, suggesting that S. flexneri and S. Typhimurium made undergo specific adaptations in response to SIgA. These findings may have implications for understanding immune surveillance in the gut. We have shown that Peyer’s patch M cells transport SIgA and SIgA-antigen complexes from the intestinal lumen to underlying dendritic cells (DC), and that the uptake of SIgA-immune complexes by DCs may be mediated by the mannose receptor and/or DC-¬SIGN. The fact that SIgA may be capable of transiently rendering S. flexneri and S. Typhimurium avirulent suggests a mechanism by which the normally pathogenic bacteria can be sampled safely by the mucosal immune system.
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