The anti-inflammatory properties of high-density lipoproteins (HDL) are lost in uremia.\nThese HDL may show pro-inflammatory features partially as a result of changed protein composition.\nAlterations of polymorphonuclear leukocytes (PMNLs) in chronic kidney disease (CKD) may\ncontribute to chronic inflammation and high vascular risk. We investigated if HDL from uremic\npatients is related to systemic inflammation by interfering with PMNL function. PMNL apoptosis\nwas investigated by assessing morphological features and DNA content. CD11b surface expression\nwas quantified by flow cytometry. Oxidative burst was measured via cytochrome c reduction assay.\nChemotaxis was assessed by using an under-agarose migration assay. We found that HDL from\nCKD and hemodialysis (HD) patients significantly attenuated PMNL apoptosis, whereas HDL\nisolated from healthy subjects had no effect on PMNL apoptosis. The use of signal transduction\ninhibitors indicated that uremic HDL exerts anti-apoptotic effects by activating pathways involving\nphosphoinositide 3-kinase and extracellular-signal regulated kinase. Healthy HDL attenuated the\nsurface expression of CD11b, whereas HDL from CKD and HD patients had no effect. All tested\nisolates increased the stimulation of oxidative burst, but did not affect PMNL chemotactic movement.\nIn conclusion, HDL may contribute to the systemic inflammation in uremic patients by modulating\nPMNL functions.
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