A critical role for mouse CXC chemokine(s) in pulmonary neutrophilia during th type 1-dependent airway inflammation

Ag-specific Th1 and Th2 cells have been demonstrated to play a critical rol e in the induction of allergic diseases. Here we have investigated the prec ise mechanisms of Th1-induced airway inflammation. Airway inflammation was induced in BALB/c mice by transfer of freshly induced OVA-specific Th1 or T h2 cells followed by OVA inhalation. In this model, both Th1 and Th2 cells induced airway inflammation. The former induced neutrophilia in airways, wh ereas the latter induced eosinophilia. Moreover, we found that Th1 cells in duced more severe airway hyperresponsiveness (AHR) than Th2 cells. The eosi nophilia induced by Th2 cell infusion was almost completely blocked by admi nistration of anti-IL-5 mAb, but not anti-IL-4 mAb. In contrast, Th1-induce d AHR and pulmonary neutrophilia were inhibited by the administration of an ti-human IL-8R Ab, which blocks the function of mouse CXC chemokine(s). The se findings reveal a critical role of mouse CXC chemokine(s) in Th1-depende nt pulmonary neutrophilia and AHR.