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. 2014 Sep 8;143(2):258–268. doi: 10.1111/imm.12306

Figure 4.

Figure 4

Role of MyD88 and nuclear factor-κB/activator protein 1 ((NF-κB/AP-1) in heat-killed Mycobacterium indicus pranii (MIP-K), live Mycobacterium indicus pranii (MIP-L) and bacillus Calmette–Guérin (BCG) mediated activation of macrophages. Peritoneal macrophages from MyD88−/− and wild-type mice were stimulated with MIP-K, MIP-L and BCG. Response to MIP and BCG was lost in MyD88−/− macrophages, as shown by drastically reduced levels of tumour necrosis factor-α (TNF-α) and interleukin-12 p40 (IL-12p40) in culture supernatants (a,b). Role of NF-κB/AP-1 in macrophage activation by MIP or BCG was determined by stimulating RAW-Blue cells, which express NF-κB/AP-1 inducible secreted alkaline phosphatase (SEAP). Higher levels of SEAP activity were observed in response to MIP-L (c). The role of NF-κB/AP-1 in MIP-mediated macrophage activation was determined with the help of pharmacological inhibitor. RAW 264.7 macrophages were incubated with curcumin at the indicated concentration for 30 min and then stimulated with MIP-K, MIP-L and BCG. Dose-dependent decrease in TNF-α production in response to MIP-K, MIP-L and BCG was observed in the presence of curcumin (d). Data shown are mean ± SEM of three independent experiments. *P < 0·05, **P < 0·01, ***P < 0·001 and ns, not significant.