ROS in gastrointestinal inflammation: Rescue Or Sabotage?

被引：207

作者：

Aviello, G. ^{[1
]}

Knaus, U. G. ^{[1
,2
]}

机构：

[1] Our Ladys Childrens Hosp, Natl Childrens Res Ctr, Dublin 12, Dublin, Ireland

[2] Univ Coll Dublin, Conway Inst, Sch Med, Dublin, Ireland

来源：

BRITISH JOURNAL OF PHARMACOLOGY | 2017年 / 174卷 / 12期

基金：

爱尔兰科学基金会;

关键词：

CHRONIC GRANULOMATOUS-DISEASE; REACTIVE OXYGEN METABOLITES; FORMYL PEPTIDE RECEPTOR; NADPH OXIDASE SUBUNIT; HELICOBACTER-PYLORI; OXIDATIVE STRESS; BOWEL-DISEASE; CROHNS-DISEASE; NITRIC-OXIDE; HYDROGEN-PEROXIDE;

D O I：

10.1111/bph.13428

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

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.

引用

页码：1704 / 1718

页数：15

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