Experimental lung research
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The alveolar epithelium participates in host defense through inflammatory pathways that activate NF-κB. Lung infections involving endotoxins trigger acute respiratory distress syndrome (ARDS) in adult and pediatric patients. The purpose of this study was to test the hypothesis that overexpression of NF-κB would worsen and conditional deletion of NF-κB signaling would improve endotoxin-induced lung inflammation using transgenic mouse models. ⋯ Overexpression of NF-κB targeted to the lung epithelium worsened lung inflammation and injury in response to LPS exposure while conditional deletion of NF-κB signaling reduced lung inflammation. Lung inflammation and injury were associated with increased cell apoptosis.