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Role of the Arylhydrocarbon Receptor (AhR) in the Pathology of Asthma and COPD

机译:芳烃受体(AhR)在哮喘和COPD病理中的作用

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The dioxins and dioxin-like compounds in cigarette smoke and environmental pollutants modulate immunological responses. These environmental toxicants are known to cause lung cancer but have also recently been implicated in allergic and inflammatory diseases such as bronchitis, asthma, and chronic obstructive pulmonary disease (COPD). In a novel pathway of this response, the activation of a nuclear receptor, arylhydrocarbon receptor (AhR), mediates the effects of these toxins through the arachidonic acid cascade, cell differentiation, cell-cell adhesion interactions, cytokine expression, and mucin production that are implicated in the pathogenesis and exacerbation of asthma/COPD. We have previously reported that human bronchial epithelial cells express AhR, and AhR activation induces mucin production through reactive oxygen species. This review discusses the role of AhR in asthma and COPD, focusing in particular on inflammatory and resident cells in the lung. We describe the important impact that AhR activation may have on the inflammation phase in the pathology of asthma and COPD. In addition, crosstalk of AhR signaling with other ligand-activated transcription factors such as peroxisome proliferator-activated receptors (PPARs) has been well documented.
机译:香烟烟雾和环境污染物中的二恶英和二恶英样化合物可调节免疫反应。已知这些环境毒物会导致肺癌,但最近也与变态反应性和炎性疾病有关,例如支气管炎,哮喘和慢性阻塞性肺疾病(COPD)。在这种反应的新途径中,核受体芳基碳氢化合物受体(AhR)的激活通过花生四烯酸级联反应,细胞分化,细胞间粘附相互作用,细胞因子表达和粘蛋白生成介导了这些毒素的作用。与哮喘/ COPD的发病和恶化有关。我们以前曾报道过,人类支气管上皮细胞表达AhR,并且AhR激活通过活性氧诱导粘蛋白生成。这篇综述讨论了AhR在哮喘和COPD中的作用,尤其着眼于肺部的炎症细胞和驻留细胞。我们描述了AhR激活对哮喘和COPD病理过程中炎症阶段的重要影响。此外,AhR信号与其他配体激活的转录因子(例如过氧化物酶体增殖物激活的受体(PPAR))的串扰已得到充分证明。

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