Abstract
Abstract Mast cells are thought to be important in the cause of allergic diseases, but the role of mast cells in the airway remodeling of chronic long-term asthma remains controversial. In this study, using the mast cell “nock in” strategy to get the mast cell-deficient WBB6F1-W/Wv mice (W/Wv) selectively reconstituted bone marrow-cultured mast cells (BMCMCs) from normal congenic wild-type mice (+/+) (+/+ BMCMCs→W/Wv mice), mice were employed to study the roles of mast cell in a murine asthma model. The mice were sensitized with ovalbumin (OVA) and challenged with OVA for 14 weeks. The mice were assessed airway reactivity by PenH. The lungs and trachea were stained with H-E for pathologic alteration, toluidine blue for mast cell, congo red for eosinophil, PAS for goblet cell and Masson’s-trichrome for fibrosis. Mast cells were not observed in the lungs of control and OVA-sensitized and challenged W/WV mice, but OVA-sensitization and challenge increased mast cell number in +/+ mice and +/+BMCMCs→W/Wv mice. OVA-sensitization and challenge could enhance airway reactivity, pathologic alteration, eosinophil infiltration, goblet cell hyperplasia and fibrosis in +/+ mice. The pathologic changes of OVA treated W/Wv mice were less than that of +/+ mice, but +/+BMCMCs→W/Wv mice could restore the reaction to OVA-sensitization and challenge of +/+ mice. These results indicate that the mast cell play an important role in the OVA-induced chronic murine asthma model.
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