ABSTRACT
Inappropriate induction of neutrophil apoptosis during infection could deplete neutrophil numbers and function, impairing host defense and favoring bacterial persistence. The aim of this work was to determine whether infection could promote neutrophil apoptosis by evaluating the rate of neutrophil apoptosis in sera of patients with pneumonia and healthy control patients. It also aimed at examining the role of FasL in infection induced neutrophil apoptosis. This study included 25 patients diagnosed as having pneumonia and 15 healthy controls. Neutrophil apoptosis was quantified by flow cytometry using propidium iodide and Becton Dickinson FACScalibur. The rate of apoptosis was greater for neutrophils isolated from patients with pneumonia than for healthy controls [P value, 0.000]. Patients with gram negative and severe infections exerted a higher rate of neutrophil apoptosis than patients with gram positive infection. The rate of neutrophil apoptosis was greater when subjected to sera from patients with either gram-negative or gram-positive infection than when subjected to sera from controls [P value, 0.001]. Moreover, anti-FasL antibody-neutralized infected sera attenuated the infected-serum-induced neutrophil apoptosis [P value, 0.000]. These results suggest that infection enhances neutrophil apoptosis possibly through FasL but its source needs to be determined in further studies
ABSTRACT
End-stage renal disease [ESRD] patients have high incidence of thrombotic events. The pathogenesis of the thrombophilic tendency in those patients is not clearly defined. Endothelial dysfunction and/or platetet activation may have an important role in thrombosis in ESRD. Circulating endothelial microparticles [EMPs] are circulating small fragments of plasma membranes of activated endothelial cells. Increased levels of circulating activated platelets and platelet hyperaggregability have been described in ESRD patients. Circulating platelet microparticles [PMPs] are small vesicles with procoagulant activity released from activated platelets. The aim of this study was to determine the levels of both circulating EMPs and PMPs in ESRD patients under maintenance hemodialysis therapy. Circulating levels of both EMPs and PMPs were measured by flow cytometry in platelet-poor plasma of 25 hemodialysis patients younger than 40 years old [14 females and 11 males] and 20 age-matched healthy controls. The blood samples were taken from the venous line before the start of the dialysis session. All patients were subjected to full history taking and clinical examination. Patients known to have any of the disease conditions that is known to cause endothelium and/ or platelet activation [Diabetes mellitus, systemic lupus erythematosus, cerebrovascular or ischemic heart disease] were excluded. The level of EMPs was higher in dialysis patients [45.20 +/- 11.03] than in the control subjects [25.2 +/- 13.13] with a statistically significant difference between the two groups [p=0.002]. Also, the level of PMPs showed a statistical significant difference [p=0.01] between dialysis patients and the control group [755.0 +/- 187.9 vs 576.0 +/- 117.70]. In the dialysis group, the EMPs counts were negatively correlated with platelet counts [r=-0.41; p=0.04] but were positively correlated with the pre-dialysis diastolic blood pressure [r=0.34; p=0.02], while the levels of PMPs were negatively correlated with the hemoglobin levels in the dialysis group [r=-0.41; p=0.04]. The levels of PMPs were positively correlated with the pre-dialysis systolic blood pressure [r=0.34; p=0.02] and the duration of hemodialysis therapy [r=0.4; p=0.05]. Increased concentrations of both endothelial-derived [EMPs] and platelet-derived [PMPs] were detected in hemodialysis patients. This may indicate endothelium and platelet activation or injury in ESRD patients. Further large scale studies are needed to confirm their roles in thrombotic events and their clinical implications