Sales M E, Sterin-Borda L, de Bracco M M, Rodriguez M, Narbaitz M, Borda E
CEFYBO-CONICET and School of Dentistry, University of Buenos Aires, Argentina.
Clin Exp Immunol. 1997 Nov;110(2):189-95. doi: 10.1111/j.1365-2249.1997.tb08316.x.
IgA was obtained from HIV-infected haemophilic patients and the intracellular signals triggered by its reaction with isolated rat intestinal strips were studied. HIV+ IgA stained intestinal microvilli with a granular immunofluorescence pattern and bound to the muscarinic acetylcholine receptor (mAChR), displacing the specific muscarinic cholinergic antagonist QNB in a non-competitive manner. It triggered the signals that are the consequence of mAChR stimulation in the intestine. Thus, it decreased cAMP synthesis and increased guanosine 3':5'-cyclic monophosphate (cGMP) formation and phosphoinositide (PI) turnover of the intestine. In addition, it stimulated prostaglandin E2(PGE2) synthesis by intestinal strips. Through its effect on PGE2 synthesis, HIV+ IgA could have a dual action. On the one hand, it could enhance immunosuppression at a local level, favouring pathogen growth and subsequent intestinal dysfunction. On the other hand, PGE2 could directly increase intestinal motility and electrolyte/fluid loss. Both effects could be involved in intestinal damage in AIDS.
从感染HIV的血友病患者中获取IgA，并研究其与分离的大鼠肠段反应所引发的细胞内信号。HIV阳性的IgA以颗粒状免疫荧光模式染色肠微绒毛，并与毒蕈碱型乙酰胆碱受体（mAChR）结合，以非竞争性方式取代特异性毒蕈碱胆碱能拮抗剂QNB。它触发了肠中mAChR刺激所产生的信号。因此，它降低了cAMP合成，并增加了肠中鸟苷3':5'-环磷酸（cGMP）的形成和磷酸肌醇（PI）的周转。此外，它刺激肠段合成前列腺素E2（PGE2）。通过其对PGE2合成的影响，HIV阳性的IgA可能具有双重作用。一方面，它可以在局部增强免疫抑制，有利于病原体生长及随后的肠道功能障碍。另一方面，PGE2可以直接增加肠道蠕动和电解质/液体流失。这两种效应都可能与艾滋病患者的肠道损伤有关。
