Interleukin (IL)-9 overexpression protects against alveolar fibrosis induced by crystalline silica particles. This cytokine is also involved in allergic asthma. In the present study, we examined the effect of IL-9 overexpression on the subepithelial fibrotic response, a feature of asthmatic remodeling, induced by chronic exposure to A. alternata extract. IL-9 overexpressing mice (Tg5) and their wild type counterparts (FVB) were intranasally exposed to A. alternata extract or PBS (controls) twice a week during 3 months. At the end of the allergic challenge, enhanced pause (Penh) measured in response to metacholine and fibrotic parameters, such as collagen and fibronectin lung content, were significantly higher in Tg5 compared to FVB. Staining of lung sections with Masson's Trichrome also showed more collagen fibers in peri-bronchial areas of treated Tg5 mice . A similar recruitment of inflammatory cells was observed in challenged FVB and Tg5 mice, except for eosinophils which were significantly more abundant in the lung of Tg5. High serum levels of IgE and IgG1 in both strains indicated that FVB and Tg5 developed a strong type 2 immune response. The concentration of the eosinophil chemoattractant RANTES and the pro-fibrotic mediator CTGF was higher in the BAL of challenged Tg5 than FVB. These results demonstrate a pro-fibrotic role of IL-9 in an airway remodeling model, possibly involving eosinophils and CTGF. These data also highlight a dual role of IL-9 in lung fibrosis, being anti- or pro-fibrotic depending on the alveolar or airway localization of the process, respectively.