Furebring Mia, Håkansson Lena Douhan, Venge Per, Nilsson Bo, Sjölin Jan
Department of Medical Sciences, Section of Infectious Diseases, University Hospital of Uppsala, Sweden.
Crit Care. 2002 Aug;6(4):363-70. doi: 10.1186/cc1524. Epub 2002 Jun 13.
Treatment of patients with severe sepsis with agents antagonising the effects of C5a has been proposed based on beneficial effects in animal experiments and in vitro studies demonstrating upregulation of the C5a receptor (CD88) on granulocytes by endotoxin.
CD88 expression on leukocytes from 12 patients with severe sepsis or septic shock was analysed by flow cytometer, and serum complement factors C3a and C5b-9 were measured by enzyme immunoassay techniques.
The granulocyte CD88 expression on day 1 was lowered (36; range, 2-59) in comparison with controls (63; range, 25-88) (P < 0.001), despite complement activation, while the monocyte CD88 expression was unchanged. The receptor reduction correlated significantly to the APACHE II score (r2 = 0.35, P < 0.05). The recovery of CD88 expression was slow.
In contrast to the findings in animals, it is concluded that granulocyte CD88 expression is reduced at the time when the diagnosis of severe sepsis or septic shock can clinically be made. The reason for this needs further investigation but it may be due to a previous complement activation or to cytokine effects.
基于动物实验和体外研究中的有益作用，有人提出用拮抗C5a作用的药物治疗严重脓毒症患者。这些研究表明内毒素可上调粒细胞上的C5a受体（CD88）。
采用流式细胞仪分析12例严重脓毒症或脓毒性休克患者白细胞上的CD88表达，并用酶免疫测定技术检测血清补体因子C3a和C5b-9。
尽管存在补体激活，但与对照组（63；范围25 - 88）相比，第1天粒细胞CD88表达降低（36；范围2 - 59）（P < 0.001），而单核细胞CD88表达未改变。受体减少与急性生理学及慢性健康状况评分系统II（APACHE II）评分显著相关（r2 = 0.35，P < 0.05）。CD88表达的恢复缓慢。
与动物实验结果相反，得出的结论是，在临床上能够做出严重脓毒症或脓毒性休克诊断时，粒细胞CD88表达降低。其原因需要进一步研究，但可能是由于先前的补体激活或细胞因子的作用。
