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谭年花,陈斌,彭杰,朱文芳,张茜茜.乙肝相关性慢加急性肝衰竭合并细菌感染患者Treg/Th17细胞免疫表达的研究[J].湖南中医药大学学报,2022,42(3):471-476[点击复制] |
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| 乙肝相关性慢加急性肝衰竭合并细菌感染患者Treg/Th17细胞免疫表达的研究 |
| 谭年花,陈斌,彭杰,朱文芳,张茜茜 |
| (湖南中医药大学, 湖南 长沙 410208;湖南中医药大学第一附属医院肝病科, 湖南 长沙 410007) |
| 摘要: |
| 目的 观察乙型病毒性肝炎（简称乙肝）相关性慢加急性肝衰竭（hepatitis B virus related acute-on-chronic liver failure, HBV-ACLF）合并细菌感染患者外周血调节性T细胞（regulatory T cell, Treg）和辅助性T细胞17（helper T cell 17, Th17）细胞计数及相关细胞因子免疫表达。方法 选择96例HBV-ACLF患者，依据感染情况分为有细菌感染组与无细菌感染组。采用流式细胞术检测患者外周血Treg、Th17细胞计数，细胞因子微球检测技术检测转化生长因子-β（transforming growth factor-β, TGF-β）、白介素-10（interleukin-10, IL-10）、肿瘤坏死因子-α（tumor necrosis factor-α, TNF-α）、白介素-17A（interleukin-17A, IL-17A）、白介素-23（interleukin-23, IL-23）表达，实时荧光定量PCR检测叉状头状转录蛋白3（forkhead box protein 3, Foxp3）、维甲酸相关孤核受体-γt（retinoid-related orphan nuclcar receptor-γt, ROR-γt） mRNA表达，及检测相关炎症指标[C反应蛋白（C-reactive protein, CRP）、降钙素原（procalcitonin, PCT）、内毒素（lipopolysaccharide, LPS）]水平。结果 有细菌感染组Treg细胞计数与无细菌感染组比较，差异无统计学意义（P>0.05）。与无细菌感染组比较，有细菌感染组Th17细胞计数明显升高（P<0.01）；有细菌感染组CRP、PCT、LPS水平均显著升高（P<0.01，P<0.05）；有细菌感染组Th17、TNF-α、IL-17A、IL-23、ROR-γt mRNA表达均明显上调（P<0.01，P<0.05）；有细菌感染组Foxp3 mRNA、IL-10表达均明显下调（P<0.01，P<0.05）。有细菌感染组恶化率（83.33%）显著高于无细菌感染组（11.11%）（P<0.01）。结论 HBV-ACLF患者随着病程进展，感染风险增加，其感染后存在Th17细胞优势化现象，具体机制可能与Th17细胞过度增值分化导致炎症反应失控，加重肝组织炎症反应相关。 |
| 关键词: 乙型病毒性肝炎 肝衰竭 调节性T细胞 辅助性T细胞17 细菌感染 |
| DOI：10.3969/j.issn.1674-070X.2022.03.023 |
| 投稿时间：2021-04-02 |
| 基金项目:国家自然科学基金项目（81673959）；中国人民解放军三〇二医院协作项目（2018ZX10725506-002）；湖南省中医药管理局科研计划项目（2017100）；湖南省研究生科研创新项目（CX20200799）。 |
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| Study on immune expression of Treg/Th17 cells in patients with HBV-ACLF and bacterial infection |
| TAN Nianhua,CHEN Bin,PENG Jie,ZHU Wenfang,ZHANG Qianqian |
| (Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;Department of Hepatology, The First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China) |
| Abstract: |
| Objective To observe the cell count of regulatory T cell (Treg) and helper T cell 17 (Th17) cell and the expression of related cytokines in peripheral blood of patients with hepatitis B virus related acute-on-chronic liver failure (HBV-ACLF) combined with bacterial infection. Methods 96 patients with HBV-ACLF were divided into bacterial infection group and non-bacterial infection group according to the infection. Flow cytometry was used to detect the cell count of Treg and Th17 in peripheral blood. The expression levels of transforming growth factor-β (TGF-β), interleukin-10 (IL-10), tumor necrosis factor α (TNF-α), interleukin-17A (IL-17A) and interleukin-23 (IL-23) were detected by cytometric bead array. The expression of forkhead box protein 3 (Foxp3) and retinoid-related orphan nuclcar receptor-γt (ROR-γt) mRNA were detected by real-time fluorescent quantitative PCR, and the levels of C-reactive protein (CRP）, procalcitonin (PCT） and lipopolysaccharide (LPS） were detected. Results There was no significant difference in Treg cell count between the bacterial infection group and non-bacterial infection group (P>0.05). Compared with the non-bacterial infection group, Th17 cell count in bacterial infection group was significantly increased (P<0.01), CRP, PCT and LPS were significantly increased in the bacterial infection group (P<0.01, P<0.05). The expression of Th17, TNF-α, IL-17A, IL-23 and ROR-γt mRNA in the bacterial infection group were all up-regulated (P<0.01, P<0.05), Foxp3 mRNA and IL-10 expression were significantly down-regulated in bacterial infection group (P<0.01, P<0.05). The deterioration rate in the bacterial infection group (83.33%) was significantly higher than that in the non-bacterial infection group (11.11%) (P<0.01). Conclusion Patients with HBV-ACLF have an increased risk of infection with the progression of the disease, and there is a phenomenon of Th17 cell dominance after infection. It may be related to the excessive value-added differentiation of Th17 cell, which leads to the uncontrolled inflammatory response and aggravates the inflammatory response of liver tissue. |
| Key words: viral hepatitis B liver failure regulatory T cell helper T cell 17 bacterial infection |
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