Boratyńska M
Katedra i Klinika Nefrologii Akademii Medycznej we Wrocławiu.
Pol Arch Med Wewn. 1998 Apr;99(4):272-80.
Monocyte chemotactic peptide-1 (MCP-1) plays a key role as a mediator of inflammatory infiltration, mainly composed with macrophages. Experimental studies showed that macrophages and their products are pathogenetic factors of chronic renal graft rejection (ch.g.r.). The objective of the present study was to determine the role of MCP-1 in the pathogenesis of human renal ch.g.r. Examined were 34 patients with ch.g.r. (Group I), 50 patients with a stable allograft function (Group II), and 25 healthy subjects (control). Serum and urine levels of MCP-1 were measured by ELISA. The serum level of MCP-1 was found to be higher in transplant patients, than in control group, but this difference was not significant. The serum level of MCP-1 showed a correlation with concentration of triglycerides in both transplant patient groups. This may results from overproduction of MCP-1 through cells of vascular wall affected by hyperlipidemic microenvironment. Considering the lack of relationship between the serum and urine levels of MCP-1, I decided attribute the urine levels of MCP-1 to the secretion through the infiltrating cells and through the kidney cells. In patients with ch.g.r. the urine levels of MCP-1 were significantly higher p < 0.001) than in patients with a stable graft function and control group. MCP-1 levels were particularly high (> 2000 pg/mg creatinine) in patients with enhanced dynamics of ch.g.r. The MCP-1 levels were higher in those patients whose biopsies described cellular infiltration (1385 + 820 pg/mg creatinine vs 680 + 280 pg/mg creatinine). The urine level of MCP-1 showed a correlation with concentration of serum creatinine, cholesterol, level of proteinuria and with arterial pressure in ch.g.r. patients. Increased urine levels of MCP-1 and correlation of MCP-1 with the activity of progressive deterioration of the graft function suggest important role of this chemokine in the pathogenesis of ch.g.r., possibly by activating macrophages and by stimulating their influx into the vascular wall, glomeruli and interstitial tissue. Relationship of urinary MCP-1 excretion with arterial hypertension and lipid disorder suggest that the effect of those risk factors for a progressive deterioration of graft function manifest on the molecular level by affecting the generation of MCP-1.
单核细胞趋化肽-1（MCP-1）作为炎症浸润的介质发挥关键作用，主要由巨噬细胞组成。实验研究表明，巨噬细胞及其产物是慢性肾移植排斥反应（ch.g.r.）的致病因素。本研究的目的是确定MCP-1在人类肾ch.g.r.发病机制中的作用。研究对象为34例ch.g.r.患者（I组）、50例移植肾功能稳定的患者（II组）和25名健康受试者（对照组）。采用酶联免疫吸附测定法（ELISA）检测血清和尿液中MCP-1的水平。发现移植患者血清中MCP-1水平高于对照组，但差异无统计学意义。在两个移植患者组中，MCP-1血清水平均与甘油三酯浓度相关。这可能是由于高脂血症微环境影响血管壁细胞导致MCP-1产生过多所致。考虑到MCP-1血清水平与尿液水平之间缺乏相关性，我认为尿液中MCP-1水平归因于浸润细胞和肾细胞的分泌。ch.g.r.患者尿液中MCP-1水平显著高于移植肾功能稳定的患者和对照组（p<0.001）。在ch.g.r.病情进展较快的患者中，MCP-1水平尤其高（>2000 pg/mg肌酐）。活检显示有细胞浸润的患者MCP-1水平较高（1385±820 pg/mg肌酐 vs 680±280 pg/mg肌酐）。ch.g.r.患者尿液中MCP-1水平与血清肌酐浓度、胆固醇、蛋白尿水平及动脉血压相关。尿液中MCP-1水平升高以及MCP-1与移植肾功能进行性恶化活动的相关性表明，这种趋化因子在ch.g.r.发病机制中起重要作用，可能是通过激活巨噬细胞并刺激其流入血管壁、肾小球和间质组织。尿液中MCP-1排泄与动脉高血压和脂质紊乱的关系表明，这些移植肾功能进行性恶化的危险因素通过影响MCP-1的产生在分子水平上发挥作用。
