Defective signalling in salivary glands precedes the autoimmune response in the non-obese diabetic mouse model of sialadenitis

The spontaneous non-obese diabetic (NOD) mouse model of Sjögren's syndrome provides a valuable tool to study the onset and progression of both the autoimmune response and secretory dysfunction. Our purpose was to analyse the temporal decline of salivary secretion in NOD mice in relation to the...

Descripción completa

Detalles Bibliográficos
Autores: Rosignoli, F., Roca, Valeria Ines, Meiss, R., Leceta, J., Gomariz, Roberto Luis, Perez Leiros, Claudia
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2005
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/39392
Acceso en línea:http://hdl.handle.net/11336/39392
Access Level:acceso abierto
Palabra clave:Autoimmune Response
Nitric Oxide Signalling
Nod Mice
Sialadenitis
SjÖGren'S Syndrome
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
Descripción
Sumario:The spontaneous non-obese diabetic (NOD) mouse model of Sjögren's syndrome provides a valuable tool to study the onset and progression of both the autoimmune response and secretory dysfunction. Our purpose was to analyse the temporal decline of salivary secretion in NOD mice in relation to the autoimmune response and alterations in various signalling pathways involved in saliva secretion within each salivary gland. A progressive loss of nitric oxide synthase activity in submandibular and parotid glands started at 12 weeks of age and paralleled the decline in salivary secretion. This defect was associated with a lower response to vasoactive intestinal peptide in salivary flow rate, cAMP and nitric oxide/cGMP production. No signs of mononuclear infiltrates or local cytokine production were detectable in salivary glands in the time period studied (10-16 weeks of age). Our data support a disease model for sialadenitis in NOD mice in which the early stages are characterized by defective neurotransmitter-mediated signalling in major salivary glands that precedes the autoimmune response.