NOD mice exocrinopathy: Towards a neuroimmune link

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 ear...

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Detalles Bibliográficos
Autores principales: Calafat, Mario José, Larocca, Luciana, Roca, Valeria Inés, Pérez Leirós, Claudia
Publicado: 2007
Materias:
Apoptotic acinar cells
Exocrinopathy
Macrophages
Neuroimmune
Nitric oxide
NOD mice
gamma interferon
interleukin 10
lipopolysaccharide
nitric oxide
nitrite
vasoactive intestinal polypeptide
acinar cell
animal cell
animal model
apoptosis
conference paper
controlled study
female
macrophage
mouse
nonhuman
nonobese diabetic mouse
peritoneum macrophage
priority journal
Sjoegren syndrome
stimulation
submandibular gland
Animals
Apoptosis
Cells, Cultured
Disease Models, Animal
Epithelial Cells
Epithelium
Female
Inflammation Mediators
Interferon Type II
Interleukin-10
Lipopolysaccharides
Mice
Mice, Inbred BALB C
Mice, Inbred NOD
Neuroimmunomodulation
Nitric Oxide
Peritoneum
Sjogren's Syndrome
Submandibular Gland
Vasoactive Intestinal Peptide
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10217401_v14_n3-4_p175_Calafat
http://hdl.handle.net/20.500.12110/paper_10217401_v14_n3-4_p175_Calafat
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario: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 nonobese diabetic (NOD) mouse model of SS. We have previously described a reduced salivary secretion and signaling 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 lipopolysaccharide promoted anti-inflammatory effects by inhibiting nitric oxide synthase induction as well as IL-12 and TNF-α production, while stimulating 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 as lipopolysaccharide + IFN-γ. VIP was not effective to prevent nitrite accumulation and modestly increased IL-10 levels in macrophages coincubated with acinar cells. An enhanced nitrite response of NOD glandular macrophages in basal and stimulated conditions compared to peritoneal cells is also shown. Copyright © 2007 S. Karger AG.

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