Fig. 8: Inhibition of EGFR phosphorylation switches M1 phenotype to M2 phenotype and alleviates acute lung injury induced by sepsis. | Cell Death & Disease

Fig. 8: Inhibition of EGFR phosphorylation switches M1 phenotype to M2 phenotype and alleviates acute lung injury induced by sepsis.

From: EGFR tyrosine kinase activity and Rab GTPases coordinate EGFR trafficking to regulate macrophage activation in sepsis

Fig. 8

A–E Macrophages were collected from bronchoalveolar lavage fluid of C57BL/6 mice subjected to CLP and were divided into sham-operated, CLP and CLP plus Erlotinib (100 mg/kg, gavage) pretreatmend for 2 h, and alveolar macrophages were identified with CD45 + CD11b + F4/80high. A iNOS and CD206 expression on the surface of alveolar macrophage were analyzed by flow cytometry. B Percentage of iNOS-positive alveolar macrophage is shown (n = 9). C Mean fluorescence intensity (MFI) of iNOS is shown (n = 9). D Percentage of CD206-positive alveolar macrophage is shown (n = 9). E Mean fluorescence intensity (MFI) of CD206 is shown (n = 9). F–J Mice were injected intraperitoneally with LPS (20 mg/kg) or an equal volume of PBS, after pretreatment with Erlotinib (100 mg/kg) for 2 h. F The BALF neutrophils were analyzed by flow cytometry with neutrophils markers (CD11b and Ly6G). G Percentage of CD11b + Ly6G+ positive alveolar macrophage is shown (n = 9). H Mean fluorescence intensity (MFI) of CD11b + Ly6G+ is shown (n = 9). I Immune-staining of iNOS and CD206 in Lung sections. J Lung sections were stained with hematoxylin and eosin (H&E). Scale bar, 50 μm (upper panel) and 5 μm (lower panel). The graphs depict mean ± SD based on three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001.

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