Stress hormone epinephrine increases IgA transport across respiratory epithelial surfaces.

Abstract

Secretory immunoglobulin A (sIgA) is the principle antibody produced at the respiratory surface. Respiratory sIgA levels are increased early after injury in both human and laboratory animals; the mechanisms are uncertain. Stress hormones, including epinephrine (Epi) and norepinephrine (NE), increase early after injury. In addition, respiratory epithelial cells are known to be responsive to β2-agonists. We therefore studied the effect of Epi, NE, and albuterol on IgA transport in vitro. Calu-3 respiratory epithelial cell monolayers grown in a 2-chamber cell culture system were treated for 24 hours with Epi, NE, or albuterol (10(-6)M). Dimeric IgA was added to the basal chamber of Calu-3 cells and IgA transcellular transport was indexed by recovery of SIgA in the apical chamber by enzyme-linked immunosorbent assay. In separate experiments, Klebsiella pneumoniae (10(5) colony-forming units/mL) was added to the apical chamber of treated Calu-3 cell monolayers and bacterial passage across Calu-3 cells was determined by bacterial recovery from basal chamber media. Calu-3 cells not treated with Epi, NE, or albuterol served as control. Cell monolayer integrity was confirmed by transepithelial electrical resistance. Calu-3 cells treated with Epi led to a significant increase in sIgA transport, this was associated with an increase in polyimmunoglobulin receptor expression. Calu-3 cells treated with NE or albuterol showed no statistical difference compared with control. Only cells treated with Epi led to a significant increase in pro-inflammatory cytokine expression and decrease in bacterial passage. Epinephrine is likely an early upstream signal in the enhanced IgA response at respiratory surfaces after injury.