IGA FROM HIV+ HEMOPHILIC PATIENTS TRIGGERS INTRACELLULAR SIGNALS COUPLED TO THE CHOLINERGIC SYSTEM OF THE INTESTINE

IgA was obtained from HIV-infected haemophilic patients and the intrac ellular signals triggered by its reaction with isolated rat intestinal strips were studied. HIV(+)IgA stained intestinal microvilli with a g ranular immunofluorescence pattern and bound to the muscarinic acetylc holine receptor (mAChR), displacing the specific muscarinic cholinergi c 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 mono phosphate (cGMP) formation and phosphoinositide (PI) turnover of the i ntestine. In addition, it stimulated prostaglandin E-2(PGE(2)) synthes is by intestinal strips. Through its effect on PGE(2) synthesis, HIV()IgA could have a dual action. On the one hand, it could enhance immun osuppression at a local le:vel, favouring pathogen growth and subseque nt intestinal dysfunction. On the other hand, PGE(2) could directly in crease intestinal motility and electrolyte/fluid loss. Both effects co uld be involved in intestinal damage in AIDS.