The Hypoxia-Adenosine Link during Intestinal Inflammation.

The Hypoxia-Adenosine Link during Intestinal Inflammation.
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肠炎期间缺氧 - 腺苷连接。

DOI:
10.4049/jimmunol.1701414
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发表时间:
2018-02-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Eltzschig HK
Eltzschig HK
中科院分区:
其他
文献类型:
--
作者:
Bowser JL;Phan LH;Eltzschig HK

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肠道炎症是炎症性肠病(IBD)的一个关键因素,与多种因素有关,包括遗传、粘膜屏障功能障碍、细菌易位、有害的宿主-微生物相互作用和失调的免疫反应。在过去的十年中,人们认识到这些炎症病变与严重的组织缺氧有关。有趣的是,缺氧信号控制下的内源性适应性反应是腺苷信号的增强,这会影响这些不同的终点,包括促进屏障功能和鼓励抗炎活性。在这篇综述中,我们讨论了炎症性肠病、肠道缺血/再灌注损伤和结肠癌中缺氧-腺苷的联系。此外,我们还总结了缺氧和腺苷信号传导在肠道炎症和疾病中的临床意义。
Intestinal inflammation is a key element in inflammatory bowel disease (IBD) and is related to a combination of factors, including genetics, mucosal barrier dysfunction, bacteria translocation, deleterious host-microbe interactions, and dysregulated immune responses. Over the past decade, it has been appreciated that these inflammatory lesions are associated with profound tissue hypoxia. Interestingly, an endogenous adaptive response under the control of hypoxia signaling is enhancement in adenosine signaling, which impacts these different endpoints, including promoting barrier function and encouraging anti-inflammatory activity. In this review, we discuss the hypoxia-adenosine link in IBD, intestinal ischemia/reperfusion injury, and colon cancer. Additionally, we provide a summary of clinical implications of hypoxia and adenosine signaling in intestinal inflammation and disease.
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