The relationship between CD4(+) T cell-mediated airway eosinophilic inflamm
ation and bronchial hyper-responsiveness (BHR) was investigated. Ovalbumin-
reactive T(h)o clones were adoptively transferred to unprimed BALB/c mice a
nd then the mice were challenged by inhalation of the relevant antigen, Upo
n antigen provocation, infused Th clones infiltrated into the airways, foll
owed by the accumulation and degranulation of eosinophils, goblet cell hype
rplasia, edema and increase in bronchial responsiveness to acetylcholine. T
ransfer of several clones that differed in the levels of IL-5 production re
vealed that the magnitude of in vivo eosinophilia strongly correlated with
the IL-5-producing capacity of the infused T-h clones. Administration of an
ti-IL-5 mAb almost completely suppressed antigen-induced eosinophilic infla
mmation and BHR, Administration of anti-IL-4 mAb or anti-IFN-gamma mAb enha
nced the eosinophilia and BHR, whereas anti-IL-2 mAb did not affect them, T
he number of accumulated eosinophils significantly correlated with the inte
nsity of BHR, Our present results clearly demonstrated that CD4(+) T cells
induced BHR as a result of eosinophilic inflammation: IL-5 totally regulate
d both responses.