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目的:评价IL-17在黏附侵袭性大肠杆菌感染小鼠结肠过程中的作用及其可能机制。方法:选择野生型及IL-17基因敲除的SPF级C57BL/6小鼠并随机分成4组,分别给予不同的处理:(1)野生小鼠+单纯蒸馏水灌胃处理组;(2)野生小鼠+E.coli LF82(1×109/CFU/只)灌胃10天处理组;(3)IL-17敲除小鼠+单纯蒸馏水灌胃处理组;(4)IL-17敲除小鼠+E.coli LF82灌胃10天处理组。从以下5个方面评价各组小鼠的炎症反应和IL-17水平:(1)组织病理评分评估炎症反应严重程度;(2)透射电镜下观察结肠上皮细胞的超微结构;(3)免疫组织化学检测结肠分泌的IL-17;(4)PCR检测小鼠结肠中IL-17m RNA表达;(5)ELISA检测结肠组织中IL-17的含量。结果:定植了E.coli LF82的IL-17敲除小鼠肠道炎症程度和超微结构损伤较野生型小鼠更加严重(P<0.05)。与未经E.coli LF82处理组相比,定植了E.coli LF82的野生小鼠肠道中IL-17m RNA和IL-17含量明显升高(P<0.05)。结论:IL-17在E.coli LF82在黏附侵袭结肠粘膜过程中的保护作用,IL-17是针对AIEC菌株E.coli LF82免疫的重要效应物,而结肠局部分泌增加的IL-17会改善感染的结果。
OBJECTIVE: To evaluate the role of IL-17 in the process of adhesion colonization in mice infected with invasive Escherichia coli and its possible mechanism. Methods: SPF C57BL / 6 mice with wild-type and IL-17 knockout were selected and randomly divided into 4 groups, which were given different treatments: (1) wild mice + distilled water alone group; (2) wild Mice were treated with E.coli LF82 (1 × 109 / CFU / mouse) for 10 days; (3) IL-17 knockout mice + distilled water alone group; Rats + E.coli LF82 gavage 10 days treatment group. The inflammatory response and IL-17 level in each group were evaluated from the following five aspects: (1) histopathological score to assess the severity of inflammatory reaction; (2) ultrastructure of colonic epithelial cells under transmission electron microscope; (3) immunization Histochemical detection of colonic secretion of IL-17; (4) PCR detection of colonic IL-17mRNA expression in mice; (5) ELISA detection of colonic IL-17 content. RESULTS: Intestinal inflammation and ultrastructural damage were more severe in IL-17 knockout mice colonized with E. coli LF82 than in wild type mice (P <0.05). Compared with the control group without E.coli LF82, the intestinal tract of E. coli LF82 colonized with IL-17m RNA and IL-17 significantly increased (P <0.05). CONCLUSION: The protective effect of IL-17 in the adhesion and invasion of colonic mucosa in E.coli LF82 is an important effector of AIEC strain E.coli LF82, while the increased secretion of IL-17 in the colon can improve the infection the result of.