Involvement of interleukin-1, prostaglandins and mast cells in rectal distension-induced colonic water secretion in rats
Corresponding author V. Theodorou: Institut National de la Recherche Agronomique, Pharmacology and Toxicology Unit, 180 chemin de Tournefeuille, BP 3, F-31931 Toulouse, France. Email: email@example.com
- 1In vivo rectal distension (RD) induces a neurally mediated colonic net water hypersecretion in rats. Interleukin-1β (IL-1β) also induces neural colonic water hypersecretion involving the release of prostaglandins (PGs) and a mast cell degranulation in rats. This study investigated in vivo the role of IL-1, PGs and mast cells in RD-induced colonic hypersecretion.
- 2Proximal colonic net water flux was determined using [14C]polyethylene glycol (PEG) 4000 (mol. wt, 4000) in anaesthetized rats. On strips taken from the distal colon: (i) a histological analysis was performed to determine the number of mucosal mast cells (MMC); and (ii) histamine levels were measured by radioimmunoassay after stimulation with compound 48/80.
- 3RD induced a net colonic water secretion that was blocked by i.c.v. administration of IL-1ra (an IL-1 receptor antagonist) and indomethacin, and by systemic treatment with doxantrazole and indomethacin. RD decreased the number of resident mast cells and the release of histamine from the distal colonic strips. Moreover, using SDS-PAGE immunoblotting the expression of IL-1β was detected in the brain.
- 4These results suggest that, in rats, RD induces colonic net water hypersecretion by the activation of a neuro-immunological reflex pathway, involving brain IL-1β, PG release and peripheral mast cell degranulation.