Parasympathetic modulation of local acute inflammation in murine submandibular glands.

The parasympathetic nervous system controls submandibular glands (SMG) functions in physiological and pathological conditions via muscarinic acetylcholine receptors (mAchR). We had previously demonstrated that IFNgamma and carbachol stimulate amylase secretion in normal murine SMG by mAchR activation. While the cytokine action depended on nitric oxide synthase activation, the effect of the agonist was mediated by prostaglandin E2 (PGE2) production. Both IFNgamma and carbachol triggered IFNgamma secretion in SMG. We here show that during local acute inflammation (LAI) induced by intraglandular injection of bacterial endotoxin, lypopolisaccharide (LPS), amylase secretion is decreased in comparison to control glands. We also observed that the muscarinic agonist carbachol stimulates in a dose-dependent manner amylase activity by M2 and M3 mAchR activation. Moreover, cyclooxygenase-2 (COX-2) activation and subsequent PGE2 liberation, in a nitric oxide independent manner, seem to be involved in M3 and M2 receptor activation by carbachol. In contrast, the addition of exogenous IFNgamma or carbachol inhibits the cytokine liberation in LAI glands.