Cholinergic Autoantibodies from Primary Sjögren’s Syndrome Inhibit Mucin Production via Phospholipase C and Cyclooxygenase-2 In the Rat Submandibular Gland

PASSAFARO D, STERIN-BORDA L, REINA S, BORDA E

Dental Research Journal

Dental Research Journal

Año: 2011 vol. 3 p. 138 - 145

2008-0255

Background: We demonstrated that patients with primary Sjögren’s syndrome (pSS) produce functional IgG autoantibodies that interact with the glandular M3 muscarinic acetylcholine receptors (mAChR). Methods: Mucin release and production, prostaglandin E2 (PGE2), and total inositol phosphates (InsP) were measured in rat submandibular gland in the presence of pSS IgG autoantibodies. Results: The autoantibodies interacting with M3 mAChR decreased mucin release and production through stimulation of phospholipase C (PLC) and cyclooxygenase-2 (COX-2). This stimulation leads to an incremental increase in InsP production and in PGE2 generation, inducing signaling through the EP2 receptors. Conclusion: IgG in patients with pSS could play a role in the pathoetiology of dry mouth, decreasing the salivary mucin and leading to a reduction in the protection of the oral tissues. Consequently, this augments the damage susceptibility of the mucosa. We demonstrated that patients with primary Sjögren’s syndrome (pSS) produce functional IgG autoantibodies that interact with the glandular M3 muscarinic acetylcholine receptors (mAChR). Methods: Mucin release and production, prostaglandin E2 (PGE2), and total inositol phosphates (InsP) were measured in rat submandibular gland in the presence of pSS IgG autoantibodies. Results: The autoantibodies interacting with M3 mAChR decreased mucin release and production through stimulation of phospholipase C (PLC) and cyclooxygenase-2 (COX-2). This stimulation leads to an incremental increase in InsP production and in PGE2 generation, inducing signaling through the EP2 receptors. Conclusion: IgG in patients with pSS could play a role in the pathoetiology of dry mouth, decreasing the salivary mucin and leading to a reduction in the protection of the oral tissues. Consequently, this augments the damage susceptibility of the mucosa.