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首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Clostridium difficile toxins A and B can alter epithelial permeability and promote bacterial paracellular migration through HT-29 enterocytes.
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Clostridium difficile toxins A and B can alter epithelial permeability and promote bacterial paracellular migration through HT-29 enterocytes.

机译：艰难梭状芽胞杆菌毒素A和B可以改变上皮通透性,促进细菌paracellular迁移通过HT-29肠上皮细胞。

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摘要

Clostridium difficile toxins A and B are the widely recognized etiologic agents of antibiotic-associated diseases ranging from diarrhea to pseudomembranous colitis. We hypothesized that C. difficile toxins may alter intestinal epithelial permeability and facilitate bacterial penetration of the intestinal epithelial barrier. Experiments were designed to clarify the effects of C. difficile toxins A and B on the flux of inert particles across HT-29 enterocyte monolayers, and to correlate these results with bacteria-enterocyte interactions. In all experiments, mature, confluent HT-29 cultures were preincubated 16 h with toxin A or B (1-100 ng/mL). To study alterations in epithelial permeability, toxin-treated enterocytes were incubated with 5 pM solutions of 10- and 40-kD inert dextran particles. Toxin A, but not toxin B, was associated with increased dextran flux through enterocyte monolayers. To study bacteria-enterocyte interactions, toxin-treated enterocytes were incubated with 10(8) Salmonella typhimurium, Proteus mirabilis, or Escherichia coli. Although numbers of internalized bacteria were generally unaffected, both toxins were associated with increased bacterial adherence, as well as increased bacterial transmigration through enterocyte monolayers. Bacterial transmigration was significantly greater using toxin A- compared to toxin B-treated enterocytes, consistent with the observation that dextran flux was significantly greater using toxin A- compared to toxin B-treated enterocytes. Thus intestinal colonization with toxigenic C. difficile may facilitate bacterial penetration of the intestinal epithelium by a mechanism involving increased permeability of the intestinal epithelial barrier.
机译：艰难梭状芽胞杆菌毒素A和B公认的病因antibiotic-associated疾病从腹泻pseudomembranous结肠炎。假设梭状芽孢杆菌毒素可能会改变肠道上皮通透性和促进肠道的细菌渗透上皮屏障。澄清和梭状芽孢杆菌毒素的影响B在HT-29惰性粒子的通量肠上皮细胞层,这些相关联结果与bacteria-enterocyte交互。所有实验,成熟,支流HT-29文化是preincubated 16 h和毒素A或B (1 - 100ng / mL)。渗透率、toxin-treated肠上皮细胞孵化10年期和40-kD 5点解决方案惰性粒子右旋糖酐。B与右旋糖酐通量增加通过肠上皮细胞层。bacteria-enterocyte交互,toxin-treated肠上皮细胞孵育10(8)沙门氏菌沙门氏菌感染、变形杆菌或大肠杆菌。通常是不受影响,毒素都是与细菌的依从性,增加有关以及增加细菌的轮回通过肠上皮细胞层。轮回明显更大的使用毒素,毒素相比B-treated肠上皮细胞,符合右旋糖酐通量的观测也显著大于使用毒素——相比对毒素B-treated肠上皮细胞。殖民与产毒素的梭状芽孢杆菌促进细菌的穿透肠上皮细胞的机制有关增加肠道的渗透率上皮屏障。

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