Chemokines (CCL3, CCL4, and CCL5) Inhibit ATP-Induced Release of IL-1β by Monocytic Cells

Figure 4

CCL3 signaling involves nicotinic acetylcholine receptors. Human monocytic U937 cells were primed with LPS (1 μg/ml, 5 h) and activated (a) with the pore-forming bacterial toxin nigericin (50 μM) or (b) with 2′(3′)-O-(4-benzoylbenzoyl)adenosine-5′-triphosphate (BzATP; 100 μM, 30 min). The release of IL-1β to the cell culture supernatant was measured by ELISA. (a) Nigericin induced the release of IL-1β by LPS-primed U937 cells, but the chemokine CCL3 (10 ng/ml) did not impair the nigericin-triggered release of IL-1β (). (b) Nicotinic antagonists mecamylamine (Mec; 100 μM), α-bungarotoxin (α-Bun; 1 μM), and strychnine (Stry; 10 μM), as well as α-conotoxins ArIB [V11L,V16D] (200 nM) and RgIA4 (200 nM), reversed the inhibitory effect of CCL3. Data are presented as individual data points, bars indicate median, and whiskers percentiles are 25 and 75.

(a)

(b)