Enterotoxigenic Escherichia coli Flagellin Inhibits TNF-Induced NF-κB Activation in Intestinal Epithelial Cells.
Enterotoxigenic Escherichia coli Flagellin Inhibits TNF-Induced NF-κB Activation in Intestinal Epithelial Cells.
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DOI：
10.3390/pathogens6020018
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发表时间：
2017-05-17
期刊：
影响因子：
--
通讯作者：
Hardwidge PR
中科院分区：
文献类型：
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作者：
Wang G;Geisbrecht BV;Rueter C;Hardwidge PR
产肠毒素大肠杆菌（ETEC）在发展中国家引起儿童腹泻。ETEC菌株产生热不稳定肠毒素（LT）和/或热稳定肠毒素（ST），并编码用于粘附肠上皮细胞的多种定植因子。我们之前发现ETEC分泌一种热稳定蛋白，我们将其命名为ETEC分泌因子（ESF），可抑制肿瘤坏死因子α（TNF）正常诱导的NF-κB活化程度。在此，我们使用快速蛋白液相色谱法（FPLC）分离ETEC上清液，并确定ETEC鞭毛蛋白是保护IκBα免受TNF刺激降解的必要和充分条件。这些数据表明，ETEC可能通过下调NF-κ B依赖性宿主反应来逃避宿主先天免疫反应的潜在新机制。
Enterotoxigenic Escherichia coli (ETEC) causes childhood diarrhea in developing countries. ETEC strains produce the heat-labile enterotoxin (LT) and/or heat-stable enterotoxins (ST) and encode a diverse set of colonization factors used for adherence to intestinal epithelial cells. We previously found that ETEC secretes a heat-stable protein we designated as ETEC Secreted Factor (ESF) that inhibits the extent of NF-κB activation normally induced by tumor necrosis factor alpha (TNF). Here we fractionated ETEC supernatants using fast protein liquid chromatography (FPLC) and determined that ETEC flagellin was necessary and sufficient to protect IκBα from degradation in response to TNF stimulation. These data suggest a potentially novel mechanism by which ETEC may evade the host innate immune response by down-regulating NF-κB-dependent host responses.