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首页> 外文期刊>Infection and immunity >Signal Transduction Pathways Involved in Enterohemorrhagic Escherichia coli-Induced Alterations in T84 Epithelial Permeability
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Signal Transduction Pathways Involved in Enterohemorrhagic Escherichia coli-Induced Alterations in T84 Epithelial Permeability

机译：肠出血性大肠杆菌诱导的T84上皮通透性改变的信号转导途径

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Enterohemorrhagic Escherichia coli (EHEC) infection is associated with watery diarrhea and can lead to complications, including hemorrhagic colitis and the hemolytic-uremic syndrome. The mechanisms by which these organisms produce diarrheal disease remain to be elucidated. Changes in T84 epithelial cell electrophysiology were examined following EHEC infection. T84 cell monolayers infected with EHEC O157:H7 displayed a time-dependent decrease in transepithelial resistance. Increases in the transepithelial flux of both [3H]mannitol and 51Cr-EDTA accompanied the EHEC-induced decreases in T84 resistance. Altered barrier function induced by EHEC occurred at the level of the tight junction since immunofluorescent staining of the tight-junction-associated protein ZO-1 was disrupted when examined by confocal microscopy. Decreased resistance induced by EHEC involved a protein kinase C (PKC)-dependent pathway as the highly specific PKC inhibitor, CGP41251, abrogated the EHEC-induced drop in resistance. PKC activity was also increased in T84 cells infected with EHEC. Calmodulin and myosin light chain kinase played a role in EHEC-induced resistance changes as inhibition of these effector molecules partially reversed the effects of EHEC on barrier function. These studies demonstrate that intracellular signal transduction pathways activated following EHEC infection link the increases in T84 epithelial permeability induced by this pathogen.
机译：肠出血性大肠杆菌（EHEC）感染与水样腹泻有关，并可能导致并发症，包括出血性结肠炎和溶血性尿毒症综合征。这些生物体引起腹泻病的机制仍有待阐明。 EHEC感染后检查T84上皮细胞电生理学的变化。感染EHEC O157：H7的T84细胞单层细胞的跨上皮抵抗力呈时间依赖性下降。 [ 3 H]甘露醇和 51 Cr-EDTA的跨上皮通量增加，伴随着EHEC诱导的T84抗性降低。由EHEC诱导的屏障功能改变发生在紧密连接的水平，因为当通过共聚焦显微镜检查时紧密连接相关蛋白ZO-1的免疫荧光染色被破坏。 EHEC诱导的耐药性降低涉及蛋白激酶C（PKC）依赖性途径，因为高度特异性的PKC抑制剂CGP41251消除了EHEC诱导的耐药性下降。在感染了EHEC的T84细胞中，PKC活性也增加了。钙调蛋白和肌球蛋白轻链激酶在EHEC诱导的耐药性变化中起作用，因为这些效应分子的抑制部分逆转了EHEC对屏障功能的作用。这些研究表明，在EHEC感染后激活的细胞内信号转导通路将这种病原体诱导的T84上皮通透性增加联系起来。

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