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首页> 外文期刊>American Journal of Physiology >Developmentally regulated tumor necrosis factor-alpha induced nuclear factor-kappaB activation in intestinal epithelium.
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Developmentally regulated tumor necrosis factor-alpha induced nuclear factor-kappaB activation in intestinal epithelium.

机译：发育调节肿瘤坏死因子-α诱导肠上皮细胞核因子-κB活化。

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摘要

Premature infants are susceptible to many conditions that are inflammatory in nature. For this patient population, which is expecting the intrauterine environment, pathways necessary for fetal life and development may not have completed the transitions necessary for extrauterine life. In this study, responses to tumor necrosis factor-alpha were compared in human fetal and adult intestinal epithelial cell lines along with preweaned and postweaned mouse intestinal sections to identify a potential developmental difference that may explain the heightened inflammatory response of preterm infants. The nuclear factor-kappaB (NF-kappaB) pathway regulates a wide variety of genes involved in immune and inflammatory processes. We report that, compared with adult intestinal epithelial cells, immature intestinal epithelial cells have increased NF-kappaB activity associated with increased NF-kappaB-DNA binding and transcriptional activity. This increased activity appears due to inadequate inhibition of signaling leading to NF-kappaB activation since there is also increased phosphorylation, ubiquitination, and degradation of the inhibitor of NF-kappaB in conjunction with decreased baseline expression and delayed resynthesis of this inhibitor. Thus we demonstrate a potential mechanism for the heightened inflammatory response of immature intestinal epithelial cells.
机译：早产婴儿易患多种自然发炎的疾病。对于期待子宫内环境的这一患者人群，胎儿生命和发育所必需的途径可能尚未完成子宫外生命所必需的过渡。在这项研究中，比较了人类胎儿和成年肠道上皮细胞系以及断奶前和断奶后小鼠肠道切片对肿瘤坏死因子-α的反应，以确定可能的发育差异，这可以解释早产儿炎症反应增强。核因子-κB（NF-kappaB）通路调节免疫和炎症过程中涉及的多种基因。我们报告，与成人肠上皮细胞相比，未成熟的肠上皮细胞具有增加的NF-kappaB活性与增加的NF-kappaB-DNA结合和转录活性。由于不充分抑制导致NF-kappaB活化的信号传导，因此出现这种增加的活性，这是因为NF-kappaB抑制剂的磷酸化，泛素化和降解增强，同时基线表达降低和该抑制剂的重新合成。因此，我们证明了未成熟的肠上皮细胞炎症反应增强的潜在机制。

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