Fig. 8
From: PM2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis
Signaling pathways involved in the inhibition of pneumococcus-induced chemokine production by PM2.5. RAW264.7 cells were pretreated with 20 μM PD98059 (Erk inhibitor) and exposed to PM2.5 (20 μg/ml) for 24 h, followed by pneumococcus infection (MOI = 10) for 6 h. Cell lysates were prepared and analyzed by western blotting using antibodies against (a) iNOS, HMGB1, p-Erk, t-Erk, and CXCR3. β-actin was used as a loading control. Relative expression levels were normalized to those in the mock-treated group and are indicated under each band. b nitric oxide concentrations were determined using Griess reagent, and (c) sHMGB1 production was assessed by ELISA. The data are means ± standard deviations from triplicate independent experiments. Statistical significance was evaluated using one-way ANOVA, followed by a post-hoc test (*, P < 0.05)