Nkambule Bongani B, Davison Glenda, Ipp Hayley
Divisions of Haematology, Department of Pathology, Stellenbosch University and NHLS, Tygerberg, South Africa.
Department of Biomedical Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Bellville, South Africa.
J Thromb Thrombolysis. 2015 Nov;40(4):458-67. doi: 10.1007/s11239-015-1212-8.
Platelet aggregates play a crucial role in the immune defence mechanism against viruses. Increased levels of lipopolysaccharide have been reported in human immunodeficiency virus (HIV) infected individuals. Platelets are capable of interacting with bacterial LPS and subsequently forming platelet leukocyte aggregates (PLAs). This study aimed at determining the levels of circulating PLAs in treatment naïve HIV infected individuals and correlating them, with markers of immune activation, disease progression and platelet aggregation. Thirty-two HIV negative and 35 HIV positive individuals were recruited from a clinic in the Western Cape. Platelet monocyte and platelet neutrophil aggregates were measured using flow cytometry at baseline and were correlated with markers of platelet activation (CD62P); aggregation (CD36); monocyte and neutrophil activation (CD69); monocyte tissue factor expression (CD142); immune activation (CD38 on T+ cells); D-dimers (a marker of active coagulation); CD4 count and viral load. Platelet monocyte aggregates were also measured post stimulation with lipopolysaccharide. PMA levels were higher in HIV 25.26 (16.16-32.28) versus control 14.12 (8.36-18.83), p = 0.0001. PMAs correlated with %CD38/8 expression (r = 0.54624, p = 0.0155); CD4 count (r = -0.6964, p = 0.0039) viral load (r = 0.633, p < 0.009) and monocyte %CD69 expression (r = 0.757, p = 0.030). In addition the %PMAs correlated with platelet %CD36 (r = 0.606, p = 0.017). The HIV group showed increased levels of %CD62P 5.44 (2.72-11.87) versus control 1.15 (0.19-3.59), p < 0.0001; %CD36 22.53 (10.59-55.15) versus 11.01 (3.69-26.98), p = 0.0312 and tissue factor (CD142) MFI 4.84 (4.01-8.17) versus 1.74 (1.07-9.3), p = 0.0240. We describe increased levels of circulating PMAs which directly correlates with markers of immune activation, disease progression and platelet aggregation in HIV treatment naïve individuals.
血小板聚集体在抗病毒免疫防御机制中发挥着关键作用。据报道，人类免疫缺陷病毒（HIV）感染者体内脂多糖水平升高。血小板能够与细菌脂多糖相互作用，随后形成血小板白细胞聚集体（PLA）。本研究旨在测定初治HIV感染者循环中PLA的水平，并将其与免疫激活、疾病进展和血小板聚集的标志物相关联。从西开普省的一家诊所招募了32名HIV阴性和35名HIV阳性个体。在基线时使用流式细胞术测量血小板单核细胞聚集体和血小板中性粒细胞聚集体，并将其与血小板激活标志物（CD62P）、聚集标志物（CD36）、单核细胞和中性粒细胞激活标志物（CD69）、单核细胞组织因子表达（CD142）、免疫激活标志物（T + 细胞上的CD38）、D - 二聚体（活性凝血标志物）、CD4计数和病毒载量相关联。还用脂多糖刺激后测量血小板单核细胞聚集体。HIV组的PMA水平为25.26（16.16 - 32.28），而对照组为14.12（8.36 - 18.83），p = 0.0001。PMA与%CD38/8表达相关（r = 0.54624，p = 0.0155）；CD4计数（r = -0.6964，p = 0.0039）、病毒载量（r = 0.633，p < 0.009）和单核细胞%CD69表达相关（r = 0.757，p = 0.030）。此外，%PMA与血小板%CD36相关（r = 0.606，p = 0.017）。HIV组的%CD62P水平为5.44（2.72 - 11.87），而对照组为1.15（0.19 - 3.59），p < 0.0001；%CD36为22.53（10.59 - 55.15），而对照组为11.01（3.69 - 26.98），p = 0.0312；组织因子（CD142）平均荧光强度（MFI）为4.84（4.01 - 8.17），而对照组为1.74（1.07 - 9.3），p = 0.0240。我们描述了初治HIV感染者循环中PMA水平升高，其与免疫激活、疾病进展和血小板聚集的标志物直接相关。
