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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: NOX2 deficiency alters macrophage phenotype through an IL-10/STAT3 dependent mechanism: implications for traumatic brain injury

Fig. 4

IL-10 production and downstream effectors are elevated in NOX2−/− BMDMs in response to LPS/IL-4. (a) LPS/IL-4 (both 10 ng/ml; 24 h) stimulation significantly increased IL-10 protein concentration in WT and NOX2−/− BMDMs (*** P < 0.001; ANOVA). The LPS/IL-4-induced increase in IL-10 concentration was significantly increased in NOX2−/− BMDMs compared with WT BMDMs (+++p < 0.001, WT LPS/IL-4 vs. NOX2−/− LPS/IL-4; ANOVA). (b, c) Protein expression of phosphorylated STAT3 was significantly increased in WT and NOX2−/− BMDMs following LPS/IL-4 stimulation (*** P < 0.001; ANOVA; representative western immunoblot shown in b). LPS/IL-4-induced pSTAT3 expression was significantly increased in NOX2−/− BMDMs compared with WT BMDMs (+++ P < 0.001, WT LPS/IL-4 vs. NOX2−/− LPS/IL-4; ANOVA). (d) LPS/IL-4 significantly increased IL-4Rα mRNA expression NOX2−/− BMDMs (*** P < 0.001; ANOVA). (e) SOCS3 mRNA expression was significantly increased in WT and NOX2−/− BMDMs following LPS/IL-4 stimulation (*** P < 0.001; ANOVA). LPS/IL-4-induced SOCS3 expression was significantly increased NOX2−/− BMDMs compared with WT BMDMs (+++ P < 0.001, WT LPS/IL-4 vs. NOX2−/− LPS/IL-4; ANOVA). All data are expressed as means (± SEM, n = 6)

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