Background: Similar to Th2 cell-mediated responses, Th9 cell has been shown to induce airway eosinophilic inflammation accompanied by bronchial hyperresponsiveness (BHR). However, whether the Th2- and Th9-mediated responses share the same pathogenesis is unclear. Herein, we comparatively investigated antigen-induced airway inflammation in Th2 and Th9 cell-transferred mice in view of the eosinophil dependency and steroid sensitivity.
Methods: After adoptive transfer of in vitro-differentiated ovalbumin (OVA)-specific Th2 and Th9 cells, BALB/c mice and eosinophil-deficient mice were challenged with OVA. Then the accumulation of inflammatory cells in the lungs and the bronchial responsiveness to inhaled methacholine were determined. The effect of dexamethasone on these responses was also examined.
Results: In both Th2 and Th9 cell-transferred mice, the accumulation of eosinophils in the lungs and BHR were induced by antigen challenge. The antigen-induced BHR produced by Th2 cells was significantly weaker in eosinophil-deficient mice, though that by Th9 cells was equivalent in eosinophil-deficient and wild-type mice. Dexamethasone suppressed cytokine production by Th2 and Th9 cells in vitro, though Th2 but not Th9 cell-mediated eosinophil accumulation and BHR was significantly suppressed by in vivo treatment with dexamethasone.
Conclusions: In contrast to the similar pathological features, the mechanisms underlying Th2 and Th9 cell-mediated allergic inflammation are different. Th9 cells that elicit eosinophil-independent BHR might be involved in the pathogenesis of steroid-resistant asthma.