Σπειραματικά επίπεδα και προέλευση του παράγοντα ενεργοποίησης των αιμοπεταλίων (PAF) στην πειραματική σπειραματονεφρίτιδα

Abstract

The renal glomerulus and its various cell types (i.e. mesangial cells, endothelial cells) have been shown to synthesize compounds with autacoid and proinflammatory effects. [97,98] The spectrum of proinflammatory compounds of glomerular origin has recently expanded to include the alkyl ether glycerophospholipids, including 1-O-alkyl-2- acetyl-sn- glycero-3- phosphorylcholine, which is structurally identical with platelet activating factor (PAF).This compound can induce platelet and neutrophil aggregation and chemokinesis, vasodilation, increased vascular permeability and stimulation of eicosanoid production. We have demonstrated that PAF can be both synthesized and degraded in isolated glomeruli and in mesangial cells, [7,99] the latter being also capable of de novo synthesis of PAF precursors. Recent observations indicate that PAF receptor antagonism ameliorates glomerular inflammation in rabbit nephrotoxic serum nephritis, as well as the glomerular inflammatory injury induced by in situ formation of immune complexes in the rat kidney with experimental passive reverse Arthus reaction. [100,101] The present study was undertaken in order to assess the levels and cellular sources of glomerular PAF in glomeruli isolated from rats with: 1) Nephrotoxic serum nephritis, an infiltrative and complement dependent model of immune injury and 2) passive Heymann nephritis a non- infiltrative but complement dependent model. The role of complement, platelets and polymorphonuclear leucocytes was assessed. The observation that mesangial cells is the main source of PAF production in the rat glomerulus, prompted the assessment of the effect of various inflammatory mediators on the acetyl-transferase activity of the mesangial cells. […]