Diabetic subjects have a higher infective risk than healthy people, with more frequent and severe infections. This predisposition to infections is determined by hyperglycemia, microangiopathy and altered immune system. In particular, there is a polymorphonuclear leukocytes disfunction including chemotaxis, phagocytosis, bacterial killing and cellular activation by infective stimulus. These alterations are due to abnormal properties of polymorphonuclear leukocytes (PMN) in diabetic patients. Several parameters like phagocytosis of bacterial cells, chemiluminescence during oxidative burst and cell membrane deformability are related to glycaemia and glycated hemoglobin. Recent acquisitions show an altered integrin pattern on diabetics PMN, at baseline and after in vitro stimulation with soluble stimulus like fMLP or PMA. This could influence the interactions between PMN and endothelial cells and the diapedesis. Receptorial alterations on PMN surface may be ascribed to the abnormalities of the cytoscheleton, of the endocytosis and of the transduction mechanism, due to hyperglycemia.
|Stato di pubblicazione||Published - 2008|
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