Caveolin-1 plays a critical role in host immunity against Klebsiella pneumoniae by regulating STAT5 and Akt activity.

摘要: Caveolin-1 (Cav1) is a structural protein of caveolae. Although Cav1 associated with certain bacterial infections, it unknown whether involved in host immunity against Klebsiella pneumoniae, the third most commonly isolated microorganism from sepsis patients. Here, we showed that cav1 knockout mice succumbed to K. pneumoniae infection markedly decreased survival rates, increased burdens, intensified tissue injury, hyperactive proinflammatory cytokines, and systemic dissemination as compared WT mice. Knocking down by dominant negative approach lung epithelial MLE-12 cells resulted similar outcomes (decreased clearance cytokine production). Furthermore, revealed STAT5 influences GSK3β−β-catenin−Akt pathway, which contributes intensive inflammatory response rapid seen deficiency. Collectively, our findings indicate may offer resistance infection, affecting both local production cytokines via actions pathway.