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Fig. 7 | Critical Care

Fig. 7

From: Interleukin-36 is overexpressed in human sepsis and IL-36 receptor deletion aggravates lung injury and mortality through epithelial cells and fibroblasts in experimental murine sepsis

Fig. 7

Interleukin (IL)-36R signaling promotes epithelial apoptosis via NF-κB pathway. A Representative flow cytometry plots showing the frequency of epithelial cells (CD326+), in lung tissue from CLP-induced wild type and IL-36R knock out mice. Pooled flow cytometry data of the frequency of epithelial cells. B Representative flow cytometry plots showing the frequency of epithelial cells apoptosis in lung tissue from CLP-induced wild type and IL-36R knock out mice. Pooled flow cytometry data of the frequency of epithelial cells apoptosis. C Heat map of lung epithelial cells RNA-seq (n = 3) from wild type (WT) and IL-36R knock out (KO) mice after CLP 3 days. The fluorescence intensity of differentially expressed RNAs (≥ twofold) is illustrated from high (red) to low (blue). D Gene ontology (GO) analysis on differentially expressed RNAs. E Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis on differentially expressed RNAs; the 20 most enriched pathways related to signaling transduction are shown. F Representative western blot of P65 and p-P65 in the epithelial cells. Protein quantification of P65, p-P65 in the epithelial cells. Three independent experiments were performed thrice. P ≤ 0.05 were considered statistically significant. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001

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