文摘

背景:因素预防结肠粘膜入侵病原痢疾阿米巴并不理解。发病机理的关键第一步损伤诱导的变形虫坚持目标细胞介导的表面糖蛋白凝集素E变形虫。粘蛋白降解细菌通常存在于结肠内腔产生降低可溶性或细胞表面glycoconjugates糖苷酶。目的:确定糖苷酶产生的粘蛋白降解细菌,单独或结合蛋白酶在结肠内腔,可以减少E阿米巴坚持目标上皮细胞降解E阿米巴凝集素的坚持。方法:暴露的影响E阿米巴滋养子株HM1: 200: IMSS NIH粪便文化上层的液体,文化上层清液准备粘蛋白降解细菌,和腔的蛋白酶坚持中国仓鼠卵巢(CHO)细胞被确定。表面粘附凝集素E的阿米巴滋养子治疗前后糖苷酶和蛋白酶是由免疫荧光。糖苷酶和蛋白酶纯化的影响E阿米巴凝集素是由凝胶电泳。结果:E阿米巴的孵化文化上层清液制剂或蛋白酶单独不修改他们的CHO细胞粘附。然而,24小时孵化营养体与文化的上层清液一起准备胰腺蛋白酶CHO细胞粘附降低HM1: IMSS应变71.1% (p < 0.001)和200年:NIH应变95% (p < 0.05)。孵化24小时的营养体粪便提取物含有细菌和宿主水解酶减少HM1的依从性:IMSS应变69.2% (p < 0.01)和200年NIH应变83.0%。 Reduction of trophozoite adherence to CHO cells by hydrolases was promoted by 7.5 mM cycloheximide, and was reversible on incubation in an enzyme free medium. Decrease in CHO cell adherence of trophozoites was associated with decreased lectin on trophozoites as determined by immunofluorescence using a monoclonal antibody to the lectin. Purified lectin was degraded by the mixture of faecal culture supernant preparations and proteases, but not by either alone. CONCLUSIONS: Mucin degrading bacterial glycosidases and colonic luminal proteases together, but not alone, degrade the key adherence lectin on E histolytica trophozoites resulting in decreased epithelial cell adherence. These in vitro findings suggest a potential novel host defence mechanism in the human colon wherein the invasiveness of a pathogen could be curtailed by the combined actions of bacterial and host hydrolases. This mechanism may be responsible for preventing mucosal invasion by pathogenic E histolytica.