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Fig. 3 | Journal of Inflammation

Fig. 3

From: PKM2/STAT1-mediated PD-L1 upregulation on neutrophils during sepsis promotes neutrophil organ accumulation by serving an anti-apoptotic role

Fig. 3

PKM2 activity, especially its nuclear translocation, promotes neutrophil PD-L1 expression during sepsis. A Protein levels of PKM2 in peripheral neutrophils from septic patients and healthy controls were analyzed by Western blotting. β-actin was used as the loading control. The blot is representative of three independent experiments. B, C C57BL/6 J mice were injected with PBS, LPS, or pretreated with shikonin (10 mg/kg) before LPS injection. PD-L1 levels on bone marrow neutrophils from mice under different treatments were determined by flow cytometry (B) and MFI of PD-L1 on bone marrow neutrophils (C) were measured (n = 3 each group). D, E C57BL/6 J mice were injected with PBS, LPS, or pretreated with DASA-58 (25 mg/kg) before LPS injection. PD-L1 levels on bone marrow neutrophils from mice under different treatments were determined by flow cytometry. Proportion of PD-L1+ bone marrow neutrophils (D) and MFI of PD-L1 on bone marrow neutrophils (E) were measured (n = 6 each group). F, G Protein levels of PKM2 in dHL-60s subjected to LPS treatment for 2 h, 4 h, 6 h, 8 h, 10 h and 12 h were determined by Western blotting. β-actin was used as the loading control. The blot is representative of three independent experiments. H, I PD-L1 levels of untreated dHL-60s and dHL-60s subjected to LPS treatment for 6 h, pretreatment with shikonin (1uM) before LPS stimulation, or shikonin treatment alone were measured by flow cytometry (n = 3). J, K PD-L1 levels of untreated dHL-60s and dHL-60s subjected to LPS treatment for 6 h, pretreatment with DASA-58 (20uM/ml) before LPS stimulation, or DASA-58 treatment alone were measured by flow cytometry (n = 4). One-way ANOVA was performed. Data are presented as the mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. NS, not significant

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