NOD mice exocrinopathy: towards a neuroimmune link

MARIO CALAFAT; LUCIANA LAROCCA; VALERIA ROCA; CLAUDIA PEREZ LEIROS

NEUROIMMUNOMODULATION.

Año: 2007 vol. 14 p. 175 - 181

1021-7401

Sjögren’s syndrome (SS) is a chronic autoimmune disorder of exocrine glands characterized as an autoimmune exocrinopathy and more specifically as an autoimmune epithelitis. An impaired balance of neuroimmune interactions mediated by vasoactive intestinal peptide (VIP) in the target organ at early stages of disease is explored by means of the non obese diabetic (NOD) mouse model of SS. We have previously described a reduced salivary secretion and signalling upon VIP stimulation. The effect reflected a differential regulation of the neural isoform of nitric oxide synthase by calcium calmodulin kinase II and occurred prior to the appearance of detectable levels of cytokines in NOD glands. VIP acting on NOD macrophages treated with LPS promoted anti-inflammatory effects by inhibiting NOS induction, IL-12 and TNF-α production while stimulated IL-10. Here we present evidence on the ability of apoptotic acinar cells from submandibular glands of NOD mice to stimulate nitric oxide in both peritoneal and glandular macrophage pools to a similar extent than lipopolysaccharide (LPS)+IFN-g. VIP was not effective to prevent nitrite accumulation and modestly increased IL-10 levels in macrophages co-incubated with acinar cells. An enhanced nitrite response of NOD glandular macrophages in basal and stimulated conditions compared with peritoneal cells is also shown.