上皮
基因敲除
发病机制
呼吸上皮
炎症
免疫学
花生四烯酸
脂氧合酶
哮喘
花生四烯酸5-脂氧合酶
医学
生物
化学
病理
细胞培养
酶
生物化学
遗传学
作者
Ulaganathan Mabalirajan,Rakhshinda Rehman,Tanveer Ahmad,Sarvesh Kumar,Geeta Devi Leishangthem,Suchita Singh,Amit Kumar Dinda,Shyam Biswal,Anurag Agrawal,Balaram Ghosh
摘要
The mechanisms underlying asthmatic airway epithelial injury are not clear. 12/15-lipoxygenase (an ortholog of human 15-LOX-1), which is induced by IL-13, is associated with mitochondrial degradation in reticulocytes at physiological conditions. In this study, we showed that 12/15-LOX expressed in nonepithelial cells caused epithelial injury in asthma pathogenesis. While 12/15-LOX overexpression or IL-13 administration to naïve mice showed airway epithelial injury, 12/15-LOX knockout/knockdown in allergic mice reduced airway epithelial injury. The constitutive expression of 15-LOX-1 in bronchial epithelia of normal human lungs further indicated that epithelial 15-LOX-1 may not cause epithelial injury. 12/15-LOX expression is increased in various inflammatory cells in allergic mice. Though non-epithelial cells such as macrophages or fibroblasts released 12/15-LOX metabolites upon IL-13 induction, bronchial epithelia didn't release. Further 12-S-HETE, arachidonic acid metabolite of 12/15-LOX leads to epithelial injury. These findings suggested 12/15-LOX expressed in non-epithelial cells such as macrophages and fibroblasts leads to bronchial epithelial injury.
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