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Flagellin acting via TLR5 is the major activator of key signaling pathways leading to NF-κB and proinflammatory gene program activation in intestinal epithelial cells

机译:通过TLR5起作用的鞭毛蛋白是肠上皮细胞中导致NF-κB和促炎基因程序激活的关键信号通路的主要激活剂

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摘要

BackgroundInfection of intestinal epithelial cells by pathogenic Salmonella leads to activation of signaling cascades that ultimately initiate the proinflammatory gene program. The transcription factor NF-κB is a key regulator/activator of this gene program and is potently activated. We explored the mechanism by which Salmonella activates NF-κB during infection of cultured intestinal epithelial cells and found that flagellin produced by the bacteria and contained on them leads to NF-κB activation in all the cells; invasion of cells by the bacteria is not required to activate NF-κB.
机译:背景病原性沙门氏菌感染肠道上皮细胞会导致信号传导级联的激活,最终启动促炎基因程序。转录因子NF-κB是该基因程序的关键调控因子/激活因子,并被有效激活。我们探索了沙门氏菌在培养的肠上皮细胞感染过程中激活NF-κB的机制,发现细菌产生并包含在其上的鞭毛蛋白导致所有细胞中NF-κB的激活。激活NF-κB不需要细菌入侵细胞。

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