严重烧伤后细胞免疫改变及其与高迁移率族蛋白B1的相关性

目的 探讨严重烧伤患者T细胞免疫功能的变化规律及其与高迁移率组蛋白B1(HMGB1)的相关性.方法 采集35例烧伤体表总面积>30%的患者静脉血样,根据是否并发多器官功能障碍综合征(MODS)分组(MODS组13例、非MODS组22例),采集患者伤后第1、3、5、7、14、21、28大的外周静脉血,采用酶联免疫吸附试验检测血浆HMGB1水平;观察外周血T淋巴细胞增殖反应和白细胞介素2(IL-2)的产生能力,并通过流式细胞仪检测CD4+/CD8+T细胞的比值.结果 严重烧伤患者伤后第1天血浆HMGB1水平即明显升高,其中伤后第1、7、21、28天MODS组HMGB1显著高于非MODS组(P<0.05).两组间比较,外周血T淋巴细胞增殖反应和IL-2的产生能力、CIM4+/CD8+T淋巴细胞比值在伤后第1、14、21、28天MODS组显著低于非MODS组(P均<0.05).大面积烧伤患者伤后血浆HMGB1含量与细胞免疫功能指标包括T淋巴细胞增殖活性、IL-2含量、CD4+/CD8+T细胞比值呈显著负相关(P<0.05).结论 大面积烧伤后T淋巴细胞免疫功能紊乱与患者并发MODS密切相关,严重烧伤患者血浆HMGBI水平的持续升高对机体细胞免疫功能异常具有显著影响.

Change in T cell-mediated immunity and its relationship with high mobility group box-1 protein levels in extensively burned patients

Objective To investigate the change in T cell-mediated immunity and its relationship with plasma high mobility group box-1 protein(HMGB1)levels in severely burned patients.Methods Thirty-five extensively burned patients(>30% total body surface area)were included in this study,and were divided into MODS group(n=13)and non-MODS group(n=22).The blood samples were collected on post burn days 1,3,5,7,14,21 and 28.The plasma levels of HMGB1 were measured by using ELISA,and T lymphocyte proliferation response and its IL-2 production ability in peripheral blood were determined too.In addition.the ratio of CD4+/CD8+T cells were detected by using flow cytometry.Results Plasma HMGB1 levels were markedly elevated on post burn day 1 in severely burned patients,and HMGB1 level was significantly higher in MODS group than in non-MODS group(P<0.05).Lymph proliferation response and IL-2 production of T cells in peripheral blood.and the ratio of CD4+/CD8+ T cells in MODS group were markedly lower than those in non-MODS group on post burn days 1,14,21 and 28(all P<0.05).It indicated that plasma HMGB1 levels were negatively correlated to T cellular immune function parameters.including lymphocyte proliferation response,IL-2 production,and the ratio of CD4+/CD8+ T cells in extensively burned patients(all P<0.05).Conclusions Extensive burns could lead to T cellular immune dysfunction.which appears to be associated with the development of MODS.HMGB1,as an important late mediators of inflammation,might be involved in the pathogenesis of suppression of T cell-mediated immunity in these patients.