In the present study, we tried to develop a mouse model of chronic airway inflammation and remodeling induced by chronic exposure to antigen. Furthermore, the expressions of MMPs-9 and -12 were also investigated. BALB/c mice were sensitized and then repeatedly challenged with OVA every 3 days for 54 days. At the following day after the last challenge, of days 24, 39, and 54, histological changes of the airways were studied by hematoxylin-eosin and Masson's trichrome stains. The expressions of MMPs-9 and -12 were also measured by western blot. Persistent inflammatory cells infiltration and collagen deposition in the lung tissue were observed in repeatedly challenged mice. Furthermore, the expressions of MMPs-9 and -12 were increased in the airways after repeated antigen challenges. The severest inflammation was observed in the day-54 challenged group. These results suggest that MMPs-9 and -12 might be involved in the pathogenesis of chronic airway inflammation and remodeling induced by antigen exposure in mice. 1. Introduction Airway inflammation and remodeling are important features of chronic allergic airway diseases such as asthma [1]. Severe inflammatory cell infiltration into the lung tissue, airway structure changes including epithelium desquamation and abnormal, extracellular matrix (ECM) degradation are observed in the patients with chronic allergic airway diseases [2, 3]. These structure changes of the airways are thought to be the result from chronic repetitive injury to the airway wall caused by airway inflammation; however, the relationship between airway remodeling and inflammation is poorly understood. Matrix metalloproteinases (MMPs) are a family of proteinases with zinc-dependent proteolysis, which play important roles in matrix turnover [3]. MMPs, most of which are expressed in the airways, cleave a number of ECM constituents and can be broadly divided into collagenases, gelatinases, stromelysins, elastinases, and membrane-bound forms [4–6]. In particular, MMP-9 (gelatinase B) and MMP-12 (macrophage elastase), both of which are reportedly increased in the airways of asthmatic patients [7, 8], are thought to be associated with the pathogenesis of airway inflammatory diseases [9, 10]. The expressions and involvements of MMPs-9 and -12 in the pathogenesis of allergic airway disease were tried to be studied in some animal models with acute allergic airway disease [11–15]. However, the detailed involvements of MMPs-9 and -12 in the process of chronic allergic airway inflammation and airway remodeling are still to be revealed. Therefore, a
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