Passafaro Daniela, Sterin-Borda Leonor, Reina Silvia, Borda Enri
Dentist, Pharmacology Unit, School of Dentistry, Buenos Aires University, Argentina.
Dent Res J (Isfahan). 2011 Summer;8(3):138-45.
Patients with primary Sjögren's syndrome (pSS) produce functional IgG against cholinoreceptor of exocrine glands modifying their activity. The aim of the present work was to demonstrate pSS IgG antibodies (pSS IgG) interacting with M(3) muscarinic acetylcholine receptors (mAChR) of rats submandibular glands that alter mucin release and production via phospholipase C (PLC) and cyclooxigenase-2 (COX-2) pathways.
Mucin release and production of prostaglandin E2 (PGE2), and total inositol phosphates (InsP) were measured in rat submandibular gland in the presence of pSS IgG auto antibodies.
The auto antibodies interacting with M3 mAChR decreased mucin release and production through stimulation of PLC and COX-2. This stimulation leads to an incremental increase in InsP production and in PGE2 generation, inducing signalling through the prostaglandin membrane receptors subtype 2 (EP2). Moreover, the decrease in mucin production had negative correlation with PGE(2) generation and InsP accumulation.
IgG in patients with pSS could play an important role in the pathoetiology of dry mouth, decreasing the salivary mucin through the production of proinflammatory substances and leading to the reduction in the protection of the oral tissues.
原发性干燥综合征（pSS）患者会产生针对外分泌腺胆碱能受体的功能性IgG，从而改变其活性。本研究的目的是证明pSS IgG抗体（pSS IgG）与大鼠下颌下腺的M（3）毒蕈碱型乙酰胆碱受体（mAChR）相互作用，通过磷脂酶C（PLC）和环氧化酶-2（COX-2）途径改变粘蛋白的释放和产生。
在存在pSS IgG自身抗体的情况下，测量大鼠下颌下腺中粘蛋白的释放、前列腺素E2（PGE2）的产生以及总肌醇磷酸酯（InsP）。
与M3 mAChR相互作用的自身抗体通过刺激PLC和COX-2降低了粘蛋白的释放和产生。这种刺激导致InsP产生和PGE2生成的增量增加，通过前列腺素膜受体亚型2（EP2）诱导信号传导。此外，粘蛋白产生的减少与PGE（2）生成和InsP积累呈负相关。
pSS患者的IgG可能在口干的病理病因中起重要作用，通过产生促炎物质减少唾液粘蛋白，导致口腔组织保护作用降低。
