When the integrity of airway epithelium is destroyed, the ordered airway barrier no longer exists and increases sensitivity to viral infections and allergens, leading to the occurrence of airway inflammation such as asthma. Here, we found that galectinâ7 transgenic(+) mice exhibited abnormal airway structures as embryos and after birth. These abnormalities included absent or substantially reduced pseudostratified columnar ciliated epithelium and increased monolayer cells with irregular arrangement and widening of intercellular spaces. Moreover, airway tissue from galectinâ7 transgenic(+) mice showed evidence of impaired cellâcell junctions and decreased expression of zonula occludensâ1(ZOâ1) and Eâcadherin. When treated with respiratory syncytial virus (RSV) or ovalbumin (OVA), galectinâ7 transgenic(+) mice developed substantially increased bronchial epithelial detachment and apoptosis, airway smooth muscle and basement membrane thickening, and enhanced airway responsiveness. We found that Galectinâ7 localized in the cytoplasm and nucleus of bronchial epithelial cells, and that increased apoptosis was mediated through mitochondrial release of cytochrome c and upregulated JNK1 activation and expression of caspaseâ3 in galectinâ7 Tg(+) mice. These findings suggested that Galectinâ7 causes airway structural defects and destroys airway epithelium barrier, which predispose the airways to RSV or OVAâinduced epithelial apoptosis, injury, and other asthma responses.