ArticleFrontiers in immunology2025
The ATP-mediated cytokine release by macrophages is down-modulated by unconventional α9* nicotinic acetylcholine receptors.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Peptides containing SARS-CoV-2 spike-protein residues are antagonists of α7 and α9α10 nAChRs and modulate interleukin-1β release from human monocytic THP-1 cells.The Journal of biological chemistry · 2026Article
- Putative α7-selective ligands interact with α9-containing nicotinic acetylcholine receptors and modulate immune functions of human mononuclear phagocytes.Frontiers in immunology · 2026Article
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17 authors.
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Abstract
Objective: The clinical interest in mechanisms controlling the biosynthesis and release of the pro-inflammatory cytokine interleukin (IL)-1β is outstanding, as IL-1β is associated with life-threatening inflammatory diseases including hyperinflammation caused by extracellular ATP originating from damaged cells. Previously, we identified a cholinergic mechanism controlling ATP-dependent IL-1β release via metabotropic signaling of unconventional nicotinic acetylcholine receptors (nAChRs) containing subunits α7 and α9* (denoting homomeric or heteromeric α9) in monocytes. This study examines whether this mechanism is active in human macrophages (THP-1 cell-derived, peripheral blood mononuclear cell-derived, and peritoneal macrophages). Methods: Expression of nAChR subtypes ( Results: All nAChR subunits were expressed by all cells analyzed. Activation of nAChRs efficiently inhibited the ATP-mediated IL-1β release by macrophages, while ATP-independent release remained unaffected. Moreover, the nAChR agonists inhibited the release of IL-18 and IL-1α. The inhibitory effect was reversed by subunit-specific conopeptides, indicating the involvement of unconventional nAChRs containing subunits α7 and α9*. Conclusion: We conclude that the cholinergic control of ATP-mediated IL-1β release is active in human monocytes and in macrophages and that nAChR agonists can also regulate the release of IL-18 and IL-1α. This mechanism specifically regulates the ATP-induced cytokine release, without suppressing ATP-independent cytokine release. Thus, unconventional α9* nAChRs are promising therapeutic targets for ATP-induced inflammatory diseases, including sterile hyperinflammation.
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