PLCε在日本血吸虫尾蚴性皮炎中的作用机制研究  

A study on the role of PLC? in Schistosome cercarial dermatitis

作　　者：高菲[1] 张书常 陈苓苓 朱晓龙[1] 孙越[1] 章婧[1] 郭盼[1] 纪伟华[1] 朱云娟[1] 任继玲[1] 胡立志[1] 刘佩梅[1] 

机构地区：[1]天津医科大学病原生物系,天津300070 [2]咸水沽医院,天津300000

出　　处：《中国病原生物学杂志》2017年第4期335-340,共6页Journal of Pathogen Biology

基　　金：国家自然科学基金项目(No.81573075;81301360);天津医科大学基金项目(No.2013ky06)

摘　　要：目的探讨磷脂酶Cε(PLCε)在日本血吸虫(SJ)尾蚴性皮肤炎症中的作用机制。方法用日本血吸虫尾蚴感染PLCε基因敲除(KO)和PLCε野生型(WT)两组小鼠,建立Ⅰ型和Ⅳ型超敏反应模型。于感染后不同时间点提取小鼠感染处皮肤组织,部分制作冰冻组织切片,用于HE染色检查和免疫荧光染色检查;部分组织提取总RNA,采用qRTPCR方法检测相关炎症细胞因子mRNA表达水平。结果 HE染色显示,Ⅰ型超敏反应模型中PLCεKO和WT两组皮肤肥厚度和炎性细胞浸润数量差异无统计学意义(P均>0.05)。在Ⅳ型超敏反应模型,KO小鼠炎症反应显著减弱,与WT组相比皮肤增厚程度减轻(t_(48h)=5.317,P=0.000t_(72h)=10.162,P=0.000),且炎性细胞浸润数量显著减少(t_(48h)=2.888,P=0.020)。qRT-PCR检测T细胞衍生因子IL-4,IFN,IL-17及IL-23mRNA表达在WT与KO组间差异无统计学意义(IL-4:t_(24h)=0.496,P=0.625;IFN:t_(24h)=-0.035,P=0.973;IL-17:t_(24h)=0.112,P=0.938;IL-23:t_(24h)=-1.151,P=0.261)。但成纤维细胞和角质形成细胞等体细胞所诱导的炎症细胞因子IL-1α,IL-1β以及趋化因子Cxcl-1,Cxcl-2mRNA表达在KO组受抑制(IL-1α:t_(12h)=4.785,P=0.000;t_(24h)=2.109,P=0.046;IL-1β t_(6h)=3.187,P=0.004;t_(12h)=5.049,P=0.000;Cxcl-1:t_(12h)=4.858,P=0.000;Cxcl-2:t_(24h)=7.957,P=0.000)。结论 PLCε在日本血吸虫尾蚴性皮炎中通过调控体细胞的细胞因子的表达而影响炎症反应。Objective To examine the underlying mechanisms of PLCe in cercarial dermatitis induced with S. japoni cure cercariae. Methods Type I hypersensitivity （Type I） and type IV hypersensitivity （Type IV） were induced by per- cutaneously injecting S. japonicurn cercariae into wild-type （WT） PLC and PLC knock-out （KO） mice. Skin at the in- jection site was biopsied at different time points. HE staining and immunofluorescence were performed on optimal cutting temperature （OCT） embedded sections. The levels of expression of relevant cytokine mRNA were measured using qRT- PCR. Results HE staining revealed no significant differences in type I hypersensitivity in PLC KO mice and WT PLC mice （P〉0.05）. In the type IV hypersensitivity model, WT PLC mice had thicker skin （t48 h- 5. 3 17, P=-0. 000 t72 h = 10. 162, P= 0. 000） and far greater infiltration of inflammatory cells than PLC KO mice had （t4s h = 2. 888, P= 0. 020）. qRT-PCR results indicated that the levels of expression of T-cell derived factors （IL-4, IFN , IL-17, and IL-23 mRNA） did not differ significantly between WT and KO mice （IL-4： t24h =0. 496, P=0. 625; IFN ： t 24 h=--0. 035, P=0. 973; IL-17：t24 h=0. 112, P=0. 938; IL-23：t24 h=--l. 151, P=0. 261）. However, the levels of inflammatory cytokines that were mainly expressed by keratinocytes and fibroblasts decreased in KO mice. Levels of cytokines such as IL-Ia, IL-1β, Cxcl-1, and Cxcl-2 decreased significantly in PLCs KO mice compared to levels in WT PLCs mice （IL-la： t12 h--4. 785, P --0.000; tz4h=2.109, P--0.046; IL-Iβ tsh：3.187, P=0.004; t12h=5.049, P--0.000;Cxcl-I： t12h=4.858, P 0. 000 Cxcl-2.. t24 h--7. 958, P=0. 000）. This finding was consistent with the results of HE staining. Conclusion PLCa plays a crucial role in contact dermatitis induced by S. japonicum cercariae by regulating the expression of somatic cell factors.

关 键 词：尾蚴性皮炎 血吸虫 日本 磷脂酶Cε 

分 类 号：R383.24[医药卫生—医学寄生虫学]