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Clinical and Experimental Immunology logoLink to Clinical and Experimental Immunology
. 1997 Nov;110(2):189–195. doi: 10.1111/j.1365-2249.1997.tb08316.x

IgA from HIV+ haemophilic patients triggers intracellular signals coupled to the cholinergic system of the intestine

M E SALES *, L STERIN-BORDA *, M M E DE BRACCO *, M RODRIGUEZ *, M NARBAITZ *, E BORDA *
PMCID: PMC2265510  PMID: 9367401

Abstract

IgA was obtained from HIV-infected haemophilic patients and the intracellular signals triggered by its reaction with isolated rat intestinal strips were studied. HTV+ 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 die 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.

Keywords: HTV+ IgA, AIDS intestinal disease, cholinergic receptors, muscarinic signalling

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