Jc. Kips et al., INTERLEUKIN-12 INHIBITS ANTIGEN-INDUCED AIRWAY HYPERRESPONSIVENESS INMICE, American journal of respiratory and critical care medicine, 153(2), 1996, pp. 535-539
Citations number
30
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
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.