PMN= polymorphonuclear neutrophils. stronger inducer of leucocyte and endothelial adhesion, leucocyte transendothelial migration, and leucocytemediated endothelial damage. 12, 13 Homocysteine selectively changed the pattern of expression of MCP-1 and interleukin 8. 15 The homocysteine metabolite SAH specifically depressed endothelial replication in culture. 16 Since homocysteine induced some of the same cellular responses as the cytokine and inflammatory agonist tumour necrosis factor alfa (TNFα), we compared the effects of these two compounds. Homocysteine behaved differently from TNFα. 12, 13 In some functions homocysteine was less potent. In addition, SAH specifically inhibited TNFα-induced endothelial expression of the surface antigens ICAM-1, VCAM-1, and E-selectin in culture. 18

After an infarction, ischaemic myocardium is known to be infiltrated by neutrophils, eosinophils, and then by lymphocytes and monocytes. 19 Leucocyte infiltration into infarcted brain tissue has also been noted after stroke. 20 The infiltrated leucocytes become involved in tissue reorganisation. To account for these observations, I suggest that a homocysteine concentration gradient will develop from ischaemic tissue towards the normally perfused tissues. The increasing homocysteine concentration would induce local adhesion of leucocytes to the vascular endothelium. Neutrophils could then proceed up the gradient, attracted not by homocysteine itself, which we have shown is not a chemoattractant for these cells, 12 but perhaps by the neutrophil attractant interleukin 8, 21 the expression of which is induced by homocysteine. 15 As