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. 2017 Sep;57(3):324–333. doi: 10.1165/rcmb.2016-0270OC

Figure 2.

Figure 2.

Macrophages with genetic disruption of α7, β2, or β4 subunit of nicotinic acetylcholine receptor (nAChR) attenuate the immunosuppressive effect of nicotine. Bone marrow–derived macrophages (BMM) of wild-type (WT) C57BL/6 and (A) α7-nAChR knockout (KO) mice, (B) β2-nAChR KO mice, and (C) β4-nAChR KO mice were incubated with 10% CSE for 1 hour before infection with MTB H37Rv. At 1 hour (Day 0) and 2 and 4 days after infection, intracellular MTB was quantified. Data shown are the mean (±SEM) of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 compared with WT BMM + CSE. (D) [125I]epibatidine binding to detect β2 and β4 subunits of the nAChR on WT BMM. R, resistant; S, sensitive. Data shown are the mean (±SEM) of four independent experiments. *P < 0.05.