The ATP-mediated cytokine release by macrophages is down-modulated by unconventional α9* nicotinic acetylcholine receptors.

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 (CHRN

SUBMITTER: Wolf PMK 

PROVIDER: S-EPMC12598990 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature