چکیده (انگلیسی):

Background: Airway accumulation of eosinophils and bronchial hyperresponsiveness (BHR) are prominent
features of bronchial asthma, though the contribution of eosinophils to the development of BHR is
controversial. Similar to Th2 cell-mediated pathology, Th9 cells, characterized by IL-9-producing activity,
have been demonstrated to induce airway eosinophilia and BHR. In this study, we investigated the role of
eosinophils in Th9-mediated BHR by employing Th9 cell-transferred murine airway inflammation model.
Methods: Ovalbumin (OVA)-specific Th2 and Th9 cells were differentiated from CD4þ T cells of DO11.10/
RAG-2/ mice in vitro and cytokine-producing activity of those cells was examined. BALB/c mice were
adoptively transferred with Th2 or Th9 cells and challenged with OVA. Then, the number of inflammatory
cells in bronchoalveolar lavage fluid and bronchial responsiveness to inhaled methacholine were
determined.
Results: Both in Th2 and Th9 cell-transferred mice, substantial accumulation of eosinophils in the lungs
and BHR were induced by challenge with specific antigen. Nevertheless, an essential and dispensable role
of eosinophils in Th2- and Th9-mediated BHR, respectively, was demonstrated by employing eosinophildeficient
mice. The neutralization of IL-9 as well as deficiency of IL-10 in the donor cells did not affect
Th9-mediated BHR.
Conclusions: In contrast to Th2-mediated and eosinophil-dependent BHR, Th9 could induce BHR independently
from eosinophils and its characteristic cytokines, IL-9 and IL-10.