Monocytes from Sjögren's syndrome patients display increased vasoactive intestinal peptide receptor 2 expression and impaired apoptotic cell phagocytosis

HAUK V, FRACCAROLI L, GRASSO E, EIMON A, RAMHORST R, HUBSCHER O, PÉREZ LEIRÓS C

CLINICAL AND EXPERIMENTAL IMMUNOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2014 vol. 177 p. 662 - 670

0009-9104

Primary Sjögren?s syndrome (pSS) is a chronic autoimmune disorder characterized by salivary and lacrimal gland dysfunction. Salivary gland homeostasis maintenance involves multiple neural and immune regulatory circuits and a deficient control of gland homeostasis has been proposed as a triggering factor of the autoimmune response in pSS patients. Autonomic stimulation mediates vasoactive intestinal peptide (VIP) release in the glands, a pleiotropic polypeptide with pro-secretory and immunomodulatory effects. On the hypothesis that an abnormal regulation of the epithelial-immune cell interaction with induction of pro-inflammatory mediators is involved in salivary gland homeostasis loss in pSS patients, here we analyzed early events in the interaction of salivary gland epithelial cells with immune cells from pSS patients and the modulation by VIP. By means of co-cultures of peripheral blood mononuclear cells (PBMC) from individual pSS patients or control subjects with a human salivary gland epithelial cell line (HSG), we observed that cell-cell interaction induced IL-12 in pSS monocytes but not in control monocytes, whereas an increased expression of pro-inflammatory markers and reduced migration capacity was found in epithelial cells interacting with pSS but not with control PBMC. These results support that an impaired regulation of early pro-inflammatory events in the interaction of epithelial and immune cells might have a role in pSS etiopathogenesis