Fig. 4

Sepsis induces neutrophil differentiation is mediated by p38α-MSK1/-MK2 pathway. a Gene chip showed activation of MAPK and p38α pathways at 0.5 h and 1 h after LPS (1 μg/mL) stimulation. b, c q-PCR results for PD-L1 mRNA expression. Neutrophils were challenged with LPS (1 μg/mL) or pre-treated with p38i (10 μM), MSK1i (25 μM) or MK2i (20 μM) prior to LPS challenge (n = 4). d q-PCR results for PD-L1 mRNA expression. Neutrophils were challenged with LPS (1 μg/mL) or pre-treated with p38i (10 µM), P38(αβ)i (10 µM) prior to LPS challenge (n = 4). e, f Different time points after LPS (1 μg/mL) stimulation of neutrophils, the phosphorylation of p38, p38α, MSK1, MK2 and expression of PD-L1 were observed. g Western blot results of the phosphorylation of MSK1 in neutrophils which stimulated with LPS (1 μg/mL) in 12 and 24 h. P38i (10 µM), P38(αβ)i (10 µM) or MK2i (20 µM) was preloaded. h Western blot results of PD-L1 expression in neutrophils which stimulated with LPS (1 μg/mL) in 12 h. p38i (10 µM), p38(αβ)i (10 µM), MSK1i (25 µM), MK2i (20 µM) were preloaded. i inhibitors. ^#p < 0.05, ^##p < 0.01 and ^###p < 0.001, compared with control group; *p < 0.05, **p < 0.01 and ***p < 0.001, compared with LPS group. Data are mean ± SEM