Parasympathetic Modulation of Local Acute Inflammation in Murine Submandibular Glands

Inflammation - 2003
Alejandro J. Español1, Eulalia de la Torre1, María Elena Sales2,1
1Departamento de Inmunobiología, Area Investigación, Instituto de Oncología Angel H. Roffo, Universidad de Buenos Aires, Buenos Aires, Argentina
2Consejo Nacional de Investigaciones Científicas y Técnicas, Argentina

Tóm tắt

The parasympathetic nervous system controls submandibular glands (SMG) functions in physiological and pathological conditions via muscarinic acetylcholine receptors (mAchR). We had previously demonstrated that IFNγ 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 IFNγ and carbachol triggered IFNγ 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 IFNγ or carbachol inhibits the cytokine liberation in LAI glands.

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Inflammation

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