• Lawrence N Diebel, David M Liberati, Michael T White, Clement A Diglio, and William J Brown.
• Department of Surgery, Wayne State University Health Center 6-C, UHC 6-C, 4201 St. Antoine, Detroit, MI 48201, USA. ldiebel@med.wayne.edu
• Am. J. Surg. 2006 Mar 1;191(3):386-90.

BackgroundAn exaggerated inflammatory response to infections including nosocomial pneumonia may be detrimental to the host and contribute to morbidity and mortality. Both secretory immunoglobulin A (SIgA) and IgG contribute to the immune defense of respiratory surfaces. However, their relative ability to protect against invasive infections and the resultant host inflammatory response are unknown and were the basis for this study.MethodsCalu-3 cell (a respiratory epithelial cell line) monolayers were established in a Transwell system (Costar Corp., Cambridge, MA). Escherichia coli and either polyclonal SIgA or IgG were inoculated into the apical chamber and neutrophils (polymorphonuclear neutrophils) were added to the basal chamber. PMN cytotoxic potential was indexed by %CD11b expression, superoxide anion (O(2)-) production, and % elastase release. Bacterial translocation into the basal chamber was quantitated after log transformation. Calu-3 monolayer integrity was indexed by permeability to dextran fluorescein isothiocyanate.ResultsThe addition of E coli to Calu-3/polymorphonuclear cocultures led to increases in O(2)- generation, elastase release, and CD11b expression. These effects were diminished by the addition of SIgA but not IgG. A similar effect was noted with Calu-3 barrier function.ConclusionsSIgA may function to protect against microbial invasion of respiratory surfaces and protect against tissue injury from an exaggerated inflammatory response.

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