Galectin-7 overexpression destroys airway epithelial barrier in transgenic mice

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 thatgalectin-7transgenic(+) 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 fromgalectin-7transgenic(+) mice showed evidence of impaired cell-cell junctions and decreased expression of zonula occludens-1(ZO-1) and E-cadherin. When treated with respiratory syncytial virus (RSV) or ovalbumin (OVA),galectin-7transgenic(+) mice developed substantially increased bronchial epithelial detachment and apoptosis, airway smooth muscle and basement membrane thickening, and enhanced airway responsiveness. We found that Galectin-7 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 caspase-3 ingalectin-7Tg(+) mice. These findings suggested that Galectin-7 causes airway structural defects and destroys airway epithelium barrier, which predispose the airways to RSV or OVA-induced epithelial apoptosis, injury, and other asthma responses.

Automated summary

Damage to the integrity of the airway epithelium increases the risk of airway inflammation, with galectin-7 transgenic (+) mice exhibiting abnormal airway structures and cell apoptosis, leading to enhanced sensitivity and responsiveness in the airways.