Cholinoreceptor autoantibodies in Sjögren sndrome

S. Reina, B. Oman, J. M. Anaya, L. Sterin-Borda, E. Borda

Resultado de la investigación: Contribución a RevistaArtículo

11 Citas (Scopus)

Resumen

Previous studies have demonstrated that antibodies against cholinoreceptors of exocrine glands correlate with dry mouth in persons with primary Sjögren syndrome (pSS). The aim of the present investigation was to establish if serum IgG antibodies (pSS IgG) were able to interact with cholinoreceptors in rat submandibular gland-dependent stimulation of cyclo-oxygenase 2 (COX-2) mRNA expression and PGE2 production. Our findings indicated that pSS IgG-stimulating M3, M4, and M1 cholinoreceptors exerted an increase in COX-2 mRNA without affecting COX-1 mRNA expression and increased PGE2 production. Inhibitors of phospholipase A2, COX-s, L-type calcium channel currents, and Ca2+-ATPase from sarcoplasmic reticulum prevented the pSS IgG effect on PGE2 production. An ionophore of calcium mimicked pSS IgG action, suggesting a crucial role of calcium homeostasis in the cholinoreceptor-stimulated increase in PGE2 production. Moreover, the amounts of PGE2 in saliva and in sera from persons with pSS were significantly higher than in pre- or post-menopausal women. These findings illustrate the importance of autoantibodies to cholinoreceptors in the generation of chronic inflammation of target tissues in SS.
Idioma originalEnglish (US)
Páginas (desde-hasta)832-836
Número de páginas5
PublicaciónJournal of Dental Research
DOI
EstadoPublished - sep 1 2007

Huella dactilar

Sjogren's Syndrome
Autoantibodies
Dinoprostone
Immunoglobulin G
Prostaglandin-Endoperoxide Synthases
Messenger RNA
Phospholipase A2 Inhibitors
Exocrine Glands
L-Type Calcium Channels
Calcium-Transporting ATPases
Calcium Ionophores
Antibodies
Submandibular Gland
Sarcoplasmic Reticulum
Serum
Saliva
Mouth
Homeostasis
Inflammation
Calcium

Citar esto

Reina, S. ; Oman, B. ; Anaya, J. M. ; Sterin-Borda, L. ; Borda, E. / Cholinoreceptor autoantibodies in Sjögren sndrome. En: Journal of Dental Research. 2007 ; pp. 832-836.
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abstract = "Previous studies have demonstrated that antibodies against cholinoreceptors of exocrine glands correlate with dry mouth in persons with primary Sj{\"o}gren syndrome (pSS). The aim of the present investigation was to establish if serum IgG antibodies (pSS IgG) were able to interact with cholinoreceptors in rat submandibular gland-dependent stimulation of cyclo-oxygenase 2 (COX-2) mRNA expression and PGE2 production. Our findings indicated that pSS IgG-stimulating M3, M4, and M1 cholinoreceptors exerted an increase in COX-2 mRNA without affecting COX-1 mRNA expression and increased PGE2 production. Inhibitors of phospholipase A2, COX-s, L-type calcium channel currents, and Ca2+-ATPase from sarcoplasmic reticulum prevented the pSS IgG effect on PGE2 production. An ionophore of calcium mimicked pSS IgG action, suggesting a crucial role of calcium homeostasis in the cholinoreceptor-stimulated increase in PGE2 production. Moreover, the amounts of PGE2 in saliva and in sera from persons with pSS were significantly higher than in pre- or post-menopausal women. These findings illustrate the importance of autoantibodies to cholinoreceptors in the generation of chronic inflammation of target tissues in SS.",
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Cholinoreceptor autoantibodies in Sjögren sndrome. / Reina, S.; Oman, B.; Anaya, J. M.; Sterin-Borda, L.; Borda, E.

En: Journal of Dental Research, 01.09.2007, p. 832-836.

Resultado de la investigación: Contribución a RevistaArtículo

TY - JOUR

T1 - Cholinoreceptor autoantibodies in Sjögren sndrome

AU - Reina, S.

AU - Oman, B.

AU - Anaya, J. M.

AU - Sterin-Borda, L.

AU - Borda, E.

PY - 2007/9/1

Y1 - 2007/9/1

N2 - Previous studies have demonstrated that antibodies against cholinoreceptors of exocrine glands correlate with dry mouth in persons with primary Sjögren syndrome (pSS). The aim of the present investigation was to establish if serum IgG antibodies (pSS IgG) were able to interact with cholinoreceptors in rat submandibular gland-dependent stimulation of cyclo-oxygenase 2 (COX-2) mRNA expression and PGE2 production. Our findings indicated that pSS IgG-stimulating M3, M4, and M1 cholinoreceptors exerted an increase in COX-2 mRNA without affecting COX-1 mRNA expression and increased PGE2 production. Inhibitors of phospholipase A2, COX-s, L-type calcium channel currents, and Ca2+-ATPase from sarcoplasmic reticulum prevented the pSS IgG effect on PGE2 production. An ionophore of calcium mimicked pSS IgG action, suggesting a crucial role of calcium homeostasis in the cholinoreceptor-stimulated increase in PGE2 production. Moreover, the amounts of PGE2 in saliva and in sera from persons with pSS were significantly higher than in pre- or post-menopausal women. These findings illustrate the importance of autoantibodies to cholinoreceptors in the generation of chronic inflammation of target tissues in SS.

AB - Previous studies have demonstrated that antibodies against cholinoreceptors of exocrine glands correlate with dry mouth in persons with primary Sjögren syndrome (pSS). The aim of the present investigation was to establish if serum IgG antibodies (pSS IgG) were able to interact with cholinoreceptors in rat submandibular gland-dependent stimulation of cyclo-oxygenase 2 (COX-2) mRNA expression and PGE2 production. Our findings indicated that pSS IgG-stimulating M3, M4, and M1 cholinoreceptors exerted an increase in COX-2 mRNA without affecting COX-1 mRNA expression and increased PGE2 production. Inhibitors of phospholipase A2, COX-s, L-type calcium channel currents, and Ca2+-ATPase from sarcoplasmic reticulum prevented the pSS IgG effect on PGE2 production. An ionophore of calcium mimicked pSS IgG action, suggesting a crucial role of calcium homeostasis in the cholinoreceptor-stimulated increase in PGE2 production. Moreover, the amounts of PGE2 in saliva and in sera from persons with pSS were significantly higher than in pre- or post-menopausal women. These findings illustrate the importance of autoantibodies to cholinoreceptors in the generation of chronic inflammation of target tissues in SS.

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