Induction of late airway response was involved in serum antigen-specific immunoglobulin G in rats.

Abstract The antigen-induced immediate airway response (IAR) has been considered a form of bronchoconstriction mainly provoked by histamine and leukotriene C 4 /D 4 /E 4 , which are released by stimulation by antigen-specific IgE. However, the pathophysiological features of the antigen-induced late airway response (LAR) are not yet fully understood. In the present study, sensitized rats were repeatedly exposed to ovalbumin (OVA) to induce IAR and LAR, and the immunological profiles of IAR and LAR were examined. The first antigen inhalation induced only IAR but not LAR. However, the second antigen inhalation 7 days after IAR induced LAR but not IAR. Tumor necrosis factor (TNF)-α level in BALF in LAR was significantly higher than that in IAR, although there were no differences in histamine, leukotriene C 4 /D 4 /E 4 , interleukin (IL)-1β, or IL-13 levels between IAR and LAR. Serum antigen-specific IgE titer was high in both IAR and LAR, but serum antigen-specific IgG, IgG1, and IgG2a titers were dramatically high in LAR but not IAR. There were significant correlations between antigen-specific IgG, IgG1, and IgG2a titers and LAR. Interestingly, LAR could be induced in normal rats by transfer of serum from LAR rats, which exhibited high antigen-specific IgG, IgG1, and IgG2a titers. In conclusion, these findings suggest that repeated antigen inhalation converts IAR to LAR, and that LAR is a reaction triggered by antigen-specific IgG and involving TNF-α. This is the first study to directly suggest the involvement of antigen-specific IgG in the induction of LAR.