Chagasic IgG stimulates phosphoinositide hydrolysis via neurotransmitter receptor activation: role of calcium.

GORELIK G ; BORDA E; BACMAN S; CREMASCHI GA; STERIN-BORDA L

JOURNAL OF LIPID MEDIATORS

Elsevier Science Publishers

Lugar: Amsterdam; Año: 1992 vol. 5 p. 249 - 259

0921-8319

Induction of polyphosphoinositide hydrolysis in cardiac tissue by IgG from chagasic mice was assayed. BALB/c mice auricles were labelled with myo-[3H]inositol precursor and inositol phosphate production in the presence or absence of chagasic IgG and the corresponding F(ab´)2 was measured. Both chagasic IgG and F(ab´)2 but not the normal forms specifically increased phosphoinositide turnover. This increment was blocked by muscarinic cholinergic antagonists and to an even greater extent by the phospholipase C inhibitor NCDC. Moreover, calcium channel blocking agents such as diltiazem, verapamil and D-600 also exerted an inhibitory action. A muscarinic cholinergic agonist, carbachol, and the ionophore A-23187, mimicked the action of the chagasic IgG upon phosphoinositide turnover. It is concluded that murine chagasic IgG and its F(ab´)2 fragments result in stimulation of phospholipase C-mediated phosphoinositide hydrolysis through the interaction with muscarinic cholinergic receptors requiring the cytosolic calcium concentration to be raised.