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首頁> 美國衛(wèi)生研究院文獻>ISRN Toxicology >Activation of the NFκB Pathway Enhances AhR Expression in Intestinal Caco-2 Cells
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Activation of the NFκB Pathway Enhances AhR Expression in Intestinal Caco-2 Cells

機譯：NFκB途徑的激活增強了腸道Caco-2細胞中AhR的表達。

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Recent data suggest that apart from its well-known role in the regulation of xenobiotic metabolizing enzymes, AhR is also involved in inflammation. However, the influence of inflammation on AhR expression remains unknown. Here, we demonstrated that proinflammatory conditions induced by either PMA or IL-1β enhance AhR expression in Caco-2 cells. This was associated with an increase in AhR promoter activity. By means of directed mutagenesis experiments and the use of proteasome inhibitors, we demonstrated that inflammation-induced AhR expression involved the NFκB pathway but not AP-1. Moreover, conditioned media from PMA-treated Caco-2 cells were also able to induce AhR expression, and this induction was repressed by anti-IL-1β blocking antibodies. Similar results were obtained with conditioned media from PMA-treated THP-1 cells. Taken together, these data suggest that AhR could be involved in vivo in an inflammatory loop. AhR was recently suspected to be implicated in inflammatory bowel disease. Our results support this hypothesis and suggest that AhR could be a new target for inflammatory bowel disease patient management.
機譯：最新數(shù)據(jù)表明，AhR除了在調(diào)節(jié)異源生物代謝酶方面的眾所周知的作用外，還與炎癥有關(guān)。但是，炎癥對AhR表達的影響仍然未知。在這里，我們證明了由PMA或IL-1β誘導的促炎性疾病增強了Caco-2細胞中AhR的表達。這與AhR啟動子活性的增加有關(guān)。通過定向誘變實驗和蛋白酶體抑制劑的使用，我們證明了炎癥誘導的AhR表達涉及NFκB途徑，但不涉及AP-1。此外，來自PMA處理的Caco-2細胞的條件培養(yǎng)基也能夠誘導AhR表達，并且該誘導被抗IL-1β阻斷抗體抑制。用條件培養(yǎng)基從PMA處理的THP-1細胞獲得了相似的結(jié)果。綜上，這些數(shù)據(jù)表明，AhR可能在體內(nèi)參與炎癥循環(huán)。最近懷疑AhR與炎癥性腸病有關(guān)。我們的結(jié)果支持這一假設(shè)，并表明AhR可能成為炎癥性腸病患者管理的新目標。

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