INTERLEUKIN-12 INHIBITS ANTIGEN-INDUCED AIRWAY HYPERRESPONSIVENESS INMICE

The airway inflammation observed in allergic asthma is thought to be o rchestrated by an antigen-driven T-helper-2 (Th2) lymphocyte response. In vitro data indicate that the presence of interleukin-12 (IL-12) du ring the primary stimulation of T-lymphocytes with antigen favors the development of Th1 cells. The aim of the present study was to examine the effect of IL-12 in vivo on antigen-induced airway changes in a mur ine model. C57BL/6 mice were actively sensitized to ovalbumin; 14 d la ter, they were exposed daily for 7 d to aerosolized ovalbumin. This re sulted in airway eosinophilia, production of ovalbumin-specific IgE, a nd airway hyperresponsiveness to carbachol. Administration of recombin ant murine IL-12 (rmIL-12) during the active immunization prevented th ese antigen-induced changes. In contrast, administration of rmIL-12 to actively immunized mice during the daily aerosol exposure (but not at the time of immunization) abolished airway eosinophilia and hyperresp onsiveness without influencing the production of specific IgE. These r esults suggest that IL-12 can suppress antigen-induced airway changes despite the presence of circulating specific IgE.