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. 2019 Apr 4;10:664. doi: 10.3389/fimmu.2019.00664

Figure 6.

Figure 6

SLPI signaling involves nicotinic acetylcholine receptor (nAChR) subunits α7, α9, and α10. Human monocytic U937 cells were primed with LPS (1 μg/ml, for 5 h) and further stimulated with 2′(3′)-O-(4-benzoylbenzoyl)adenosine 5′-triphosphate triethylammonium salt (BzATP; 100 mM) for 30 min. (A) Application of nicotinic antagonists mecamylamin (Mec), α-bungarotoxin (α-Bun), strychnine (Stry), RgIA4, or ArIB abolished the SLPI-mediated inhibition of BzATP-induced IL-1β release; *p ≤ 0.05 significantly different compared to cells stimulated with LPS, BzATP, and SLPI. (B) Down-regulation of the expression of nAChR subunits α7, α9, or α10 by siRNA blunted the SLPI-induced inhibitory mechanism. *p ≤ 0.05 significantly different compared to cells transfected with control siRNA (con) and stimulated with LPS, BzATP and SLPI. (C) Mouse peripheral blood mononuclear cells (mPBMCs) deficient in α9 or α10 nAChR subunits stimulated with BzATP were resistant to the SLPI-mediated inhibition. The amount of IL-1β released upon stimulation with BzATP was set to 100% and the remaining values were calculated accordingly. *p ≤ 0.05 significantly different compared to mPBMCs obtained from wild-type (WT) mice stimulated with BzATP and SLPI. Experimental groups were compared by Kruskal-Wallis test followed by Mann-Whitney rank sum test.