Fig. 2: Deletion of KLF14 can significantly induce severe inflammation in murine endotoxemia and sepsis models. | Cellular & Molecular Immunology

Fig. 2: Deletion of KLF14 can significantly induce severe inflammation in murine endotoxemia and sepsis models.

From: The transcription factor KLF14 regulates macrophage glycolysis and immune function by inhibiting HK2 in sepsis

Fig. 2

A, C The deletion of KLF14 in mice decreased the survival rate of mice with LPS (20 mg/kg)-induced endotoxemia and CLP (25-gauge needle)-induced sepsis (the data are presented as the mean ± SD, n = 15, mice per group; *P < 0.05, ***P < 0.001, Kaplan–Meier survival analysis). B, D Lung tissues of mice with CLP-induced sepsis and LPS-induced endotoxemia were stained with hematoxylin and eosin (12 h; scale bars, 100 µm). E, F Immunofluorescence staining of lung sections for the macrophage marker F4/80 (red) and DAPI (blue) (12 h; scale bar, 20 µm) and G ELISA analysis of cytokines in peripheral blood from mice with CLP-induced sepsis and LPS-induced endotoxemia (the data are presented as the mean ± SD, n = 3, *P < 0.05, ***P < 0.001)

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