Effect of the leptin receptor function specifically within lung epithelium and within macrophages and neutrophils on survival, lung injury, and inflammation during influenza A infection.

<p><b>(a)</b> Representative images and <b>(b)</b> weights of <i>db/db</i>, <i>LepR^fl/fl</i>, <i>SP-C-Cre^+/+/LepR^fl/fl</i>, and <i>LysM-Cre^+/+/LepR^fl</i>^/fl mice are shown. Quantitative real-time PCR reveals appropriate knockout of the leptin receptor <b>(c)</b> within the macrophages in <i>LysM-Cre^+/+/LepR^fl</i>^/fl mice and <b>(d)</b> within the lung epithelium in <i>SP-C-Cre^+/+/LepR^fl/fl</i> mice. <i>LepR^fl/fl</i>, <i>SP-C-Cre^+/+/LepR^fl/fl</i>, and <i>LysM-Cre^+/+/LepR^fl</i>^/fl mice were inoculated with influenza A virus (500 pfu/mouse) with assessment of <b>(e)</b> mortality and <b>(f)</b> daily weight. Four days after infection with influenza A virus (500 pfu/mouse), <i>LepR^fl/fl</i>, <i>SP-C-Cre^+/+/LepR^fl/fl</i>, and <i>LysM-Cre^+/+/LepR^fl</i>^/fl mice underwent bronchoalveolar lavage for levels of <b>(g)</b> cell count, <b>(h)</b> total protein, <b>(i–k)</b> inflammatory cytokines and <b>(l)</b> lung pathology (Hematoxylin and Eosin staining).