Lung overexpression of matrix metalloproteinase-2 protects against bronchial asthma

Background: Bronchial asthma is a chronic inflammatory disease characterized by airway infiltration of inflammatory cells (eg, eosinophils, lymphocytes), and obstructive changes and hyperresponsiveness of the airways. Chronic inflammation leads to airway remodeling. Matrix metalloproteinase-2 (MMP2) is critical regulator of the extracellular matrix. The role of MMP2 in bronchial asthma is unclear. Aims and Objects: The objective of the present study was to assess the role of the MMP2 in bronchial asthma. Methods: We developed a novel MMP-2 transgenic (TG) mouse that expresses high levels of human MMP-2 in the lung. We sensitized MMP-2 TG and wild type (WT) mice with ovaalbumin eight times for two months. After sensitization, transgenic asthma groups (MMP2/OVA) and wild type asthma groups (WT/OVA) were challenged with ovaalbumin inhalation for seven days before sacrifice. Mice receiving saline instead of ovalbumin (MMP2/SAL; WT/SAL) were used as controls. We compared airway hyperresponsiveness and the levels of cytokines and cell infiltration between TG and WT mice. Results: Hypersensitivity and expression interleukins in MMP2/OVA group decreased significantly than those in WT/OVA group. Conclusion: MMP2 may have protective roles on occurance and progression of bronchial asthma.