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促红细胞生成素对慢性肾脏病补体激活的影响

Erythropoietin Effect on Complement Activation in Chronic Kidney Disease.

作者信息

Athanasiadou Virginia, Ampelakiotou Kleio, Grigoriou Eirini, Psarra Katherina, Tsirogianni Alexandra, Valsami Serena, Pittaras Theodoros, Grapsa Eirini, Detsika Maria G

机构信息

Department of Nephrology, School of Medicine, Aretaieion University Hospital, National and Kapodistrian University of Athens, 11528 Athens, Greece.

Department of Immunology and Histocompatibility, 'Evangelismos' General Hospital, 10676 Athens, Greece.

出版信息

Biomedicines. 2024 Aug 2;12(8):1746. doi: 10.3390/biomedicines12081746.

DOI:10.3390/biomedicines12081746
PMID:39200211
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11351309/
Abstract

The complement system is an important part of innate immunity. Despite its known protective role, the complement system may contribute to increased inflammation and tissue injury in cases where its balanced activation is disrupted. The kidneys have been shown to be largely affected by complement dysregulation. The aim of the present study was to investigate the effect of erythropoietin administration, on the complement system, in chronic kidney disease patients. The study involved 20 patients with CKD who received erythropoietin and measurements of levels of complement factors C3a and C5a and complement regulatory proteins (CregPs) CD55, CD46, and CD59. An increase in serum C3a and C5a levels was observed in response to EPO therapy. The increase in C3a was statistically significant ( < 0.05) and concurrent with a statistically significant decrease in CD55 in CD4 T cells ( < 0.05) and B cells ( < 0.05) and CD59 levels in CD4 and CD8 T cells ( < 0.05) at completion of EPO therapy compared with healthy controls. The above observations demonstrate that EPO induces complement activation in patients undergoing EPO therapy with a simultaneous restriction of CRegPs expression, thus possibly allowing the uncontrolled complement activation, which may contribute to tissue injury and disease progression.

摘要

补体系统是固有免疫的重要组成部分。尽管其具有已知的保护作用,但在补体系统平衡激活受到破坏的情况下,补体系统可能会导致炎症加剧和组织损伤。肾脏已被证明在很大程度上受补体失调的影响。本研究的目的是调查促红细胞生成素给药对慢性肾脏病患者补体系统的影响。该研究纳入了20例接受促红细胞生成素治疗的慢性肾脏病患者,并检测了补体因子C3a和C5a以及补体调节蛋白(CregPs)CD55、CD46和CD59的水平。促红细胞生成素治疗后观察到血清C3a和C5a水平升高。与健康对照相比,促红细胞生成素治疗结束时,C3a的升高具有统计学意义(<0.05),同时CD4 T细胞(<0.05)和B细胞(<0.05)中的CD55以及CD4和CD8 T细胞中的CD59水平具有统计学意义的下降(<0.05)。上述观察结果表明,促红细胞生成素在接受促红细胞生成素治疗的患者中诱导补体激活,同时限制补体调节蛋白的表达,从而可能导致补体不受控制的激活,这可能会导致组织损伤和疾病进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faa8/11351309/81adc5fe0c10/biomedicines-12-01746-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faa8/11351309/8e83787dbe9e/biomedicines-12-01746-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faa8/11351309/0a4d979d4ec7/biomedicines-12-01746-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faa8/11351309/440903bbaff4/biomedicines-12-01746-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faa8/11351309/81adc5fe0c10/biomedicines-12-01746-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faa8/11351309/8e83787dbe9e/biomedicines-12-01746-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faa8/11351309/0a4d979d4ec7/biomedicines-12-01746-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faa8/11351309/440903bbaff4/biomedicines-12-01746-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faa8/11351309/81adc5fe0c10/biomedicines-12-01746-g004.jpg

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