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. 2018 Jan 18;8:1115. doi: 10.1038/s41598-018-19521-9

Figure 5.

Figure 5

TLR2/4- and MyD88-dependent secretion of chemokines. (a) Significant reduction of CCL5 secretion in HMDM after 12 h exposure to SWCNT (30 µg/mL) in the presence of the TLR2/4 inhibitor, oxPAPC (30 or 60 µg/mL). oxPAPC also blocked CCL5 secretion triggered by LPS (0.1 µg/mL) in a dose-dependent manner. Furthermore, the MyD88 inhibitor, Pephinh-MYD (25 µM), but not Pepinh-Control (25 µM), reduced NF-kB p65 phosphorylation (b) and CCL5 expression (c) in cells exposed to SWCNT (30 µg/mL) for 12 h. Pephinh-MYD (25 µM) also reduced NF-kB activation and CCL5 secretion by LPS (0.1 µg/mL). NF-kB p65 phosphorylation and CCL5 expression was determined by ELISA. (d) Cytochalasin D (10 μM), an inhibitor of actin polymerization, does not affect CCL5 secretion in HMDM exposed for 12 h to SWCNT (30 µg/mL). LPS (0.1 µg/mL) was included as a control. CCL5 levels were determined by ELISA. Data shown in panels a to d are reported as mean values ± S.D. of at least three independent experiments using cells from different donors. p* < 0.05; ** < 0.01; *** < 0.001 (one-way ANOVA with post-hoc tukey’s test).