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Protective Anti‐Lipopolysaccharide Monoclonal IgA Antibodies Interferes with Salmonella Motility and Invasion of Epithelial cells, Independent of Bacterial Agglutination
Author(s) -
Mantis Nicholas John,
Forbes Stephen,
Easchmann Marissa,
Bumpus Tia
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.852.19
Subject(s) - salmonella enterica , microbiology and biotechnology , shigella flexneri , lipopolysaccharide , salmonella , secretion , mucus , antibody , biology , immunoglobulin a , immune system , motility , monoclonal antibody , serotype , microfold cell , agglutination (biology) , immunology , bacteria , immunoglobulin g , escherichia coli , genetics , ecology , biochemistry , gene
Mucosal immunity to enteric bacterial pathogens, including Salmonella enterica serovar Typhimurium ( S .Typhimurium) and Shigella flexneri is mediated by secretory IgA (SIgA) antibodies directed against bacterial lipopolysaccharide (LPS). It has long been assumed that these antibodies protect intestinal epithelial cells from microbial colonization and invasion by simply promoting bacterial agglutination and entrapment in mucus. In this study, we challenge this paradigm by demonstrating that protective, serotype‐specific, anti‐LPS monoclonal IgA antibodies (IgA mAbs) at sub‐agglutinating concentrations interfere with bacterial motility and type three‐mediated secretion of proteins necessary for invasion of epithelial cells. These effects occurred within minutes of antibody exposure and at IgA concentrations sufficient to coat less than 5% of the bacterial LPS. By scanning electron microscopy we observed anti‐LPS IgA mAbs induced dramatic morphological changes in the surface topology of the bacterial outer membranes, suggesting motility arrest and inhibition of type‐three secretion may be the result of physical changes in the LPS layer. These data reveal a novel and previously unrecognized capacity of SIgA to effectively “disarm” microbial pathogens on mucosal surfaces and render them unable to colonize or invade host intestinal epithelial cells. This work was supported by New Investigator funds from the Wadsworth Center, New York State Department of Health.