白细胞介素-17对慢性乙型肝炎患者免疫功能的影响及细胞凋亡机制研究

摘要

目的：探究白细胞介素17（IL -17）对慢性乙型肝炎患者免疫功能的影响及与 Bcl -2蛋白表达的相关性。方法分析2014年1月至2014年12月44例接受治疗的慢性乙型肝炎患者的临床资料，并列为观察组，另选取51例进行体检的健康人群作为对照组。比较两组外周血中免疫球蛋白 IgA、IgM 及 IgG 水平；比较两组血清中肿瘤坏死因子α（TNF -α）、IL -8、IL -17及 Bcl -2水平；分析观察组患者血清中 IL -17与 IgG、Bcl -2水平相关性分析。结果观察组患者外周血中 IgA（ t =2.884，P =0.005）、IgM（ t =2.657，P =0.009）、IgG（ t =5.018，P <0.001）水平明显高于对照组，差异均具有统计学意义（ P <0.005）；观察组患者血清中 IL -8（ t =12.78，P <0.001）、IL -17（ t =62.30，P<0.001）、Bcl -2（ t =4.101，P <0.001）水平明显高于对照组，差异均具有统计学意义（ P <0.05）；采用 Pearson 相关性检验分析发现，观察组患者血清中 IL -17与 IgG 呈负相关（ r =-0.399，P =0.007），与 Bcl -2水平呈显著正相关（ t=0.512，P <0.001）。结论 IL -17表达上调可能与慢性乙型肝炎患者特异性免疫功能紊乱与促进细胞凋亡机制有关。%Objective To study the effect of interleukin - 17 on immune function in and correlation with Bcl - 2 protein expression. Methods 44 case patients with chronic hepatitis B who were treated from January 2014 to December 2014 were enrolled as observation group,51 case healthy group as control group. The levels of peripheral blood IgA,IgM and IgG was compared between the two groups. The levels of serum TNF - α,IL - 8,IL - 17 and Bcl - 2 was compared between two groups. The levels of serum IL - 17 and IgG,Bcl - 2 in the observation group correlation was analyzed. Results IgA( t = 2. 884,P = 0. 005),IgM( t = 2. 657,P = 0. 009),IgG( t = 5. 018,P < 0. 001)levels in ob-servation group of patients were significantly higher than the control group,the difference was statistically significant( P < 0. 005). The serum IL- 8( t = 12. 78,P < 0. 001),IL - 17( t = 62. 30,P < 0. 001),Bcl - 2( t = 4. 101,P < 0. 001)levels in observation group were significant-ly higher than the control group,the difference was statistically significant( P < 0. 05). By using Pearson correlation test analysis,we found that IL - 17 and IgG in the observation group showed negative correlation( r = - 0. 399,P = 0. 007). Bcl - 2 levels showed significant positive corre-lation( t = 0. 512,P < 0. 001)with IL - 17. Conclusion The rising of IL - 17 expression may be associated nonspecific immune dysfunction and promotion of cell apoptosis mechanism in chronic hepatitis B patients.