胃肠道炎症中的活性氧：拯救还是破坏？
ROS in gastrointestinal inflammation: Rescue Or Sabotage?
作者信息
Aviello G, Knaus U G
机构信息
National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
Conway Institute, School of Medicine, University College Dublin, Dublin, Ireland.
出版信息
Br J Pharmacol. 2017 Jun;174(12):1704-1718. doi: 10.1111/bph.13428. Epub 2016 Mar 3.
UNLABELLED
The intestine is composed of many distinct cell types that respond to commensal microbiota or pathogens with immune tolerance and proinflammatory signals respectively. ROS produced by mucosa-resident cells or by newly recruited innate immune cells are essential for antimicrobial responses and regulation of signalling pathways including processes involved in wound healing. Impaired ROS production due to inactivating patient variants in genes encoding NADPH oxidases as ROS source has been associated with Crohn's disease and pancolitis, whereas overproduction of ROS due to up-regulation of oxidases or altered mitochondrial function was linked to ileitis and ulcerative colitis. Here, we discuss recent advances in our understanding of how maintaining a redox balance is crucial to preserve gut homeostasis.
LINKED ARTICLES
This article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc.
未标注
肠道由许多不同的细胞类型组成，这些细胞类型分别以免疫耐受和促炎信号对共生微生物群或病原体作出反应。黏膜驻留细胞或新招募的固有免疫细胞产生的活性氧（ROS）对于抗菌反应和信号通路的调节至关重要，这些信号通路包括伤口愈合过程。由于编码作为ROS来源的NADPH氧化酶的基因中的失活患者变体导致ROS产生受损，这与克罗恩病和全结肠炎有关，而由于氧化酶上调或线粒体功能改变导致的ROS过量产生与回肠炎和溃疡性结肠炎有关。在这里，我们讨论了在理解维持氧化还原平衡对维持肠道稳态至关重要方面的最新进展。
相关文章
本文是关于健康与疾病中的氧化还原生物学和氧化应激主题部分的一部分。要查看本部分中的其他文章，请访问http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc。
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