Hypoxia and Mucosal Inflammation

被引:107
作者
Colgan, Sean P. [1 ,2 ]
Campbell, Eric L. [1 ,2 ]
Kominsky, Douglas J. [2 ,3 ]
机构
[1] Univ Colorado, Sch Med, Dept Med, Aurora, CO 80045 USA
[2] Univ Colorado, Sch Med, Mucosal Inflammat Program, Aurora, CO 80045 USA
[3] Montana State Univ, Dept Microbiol & Immunol, Bozeman, MT 59717 USA
来源
ANNUAL REVIEW OF PATHOLOGY: MECHANISMS OF DISEASE, VOL 11 | 2016年 / 11卷
关键词
metabolism; inflammation; creatine; phosphocreatine; nucleotide; nucleoside; nucleotidase; mucosa; colitis; neutrophil; epithelium; murine model; ARYL-HYDROCARBON RECEPTOR; INDUCIBLE FACTOR-I; NEUTROPHIL EXTRACELLULAR TRAPS; COLLAGEN-INDUCED ARTHRITIS; CHAIN FATTY-ACIDS; PROLYL HYDROXYLASE INHIBITION; CHRONIC GRANULOMATOUS-DISEASE; INTESTINAL EPITHELIAL-CELLS; TUMOR-SUPPRESSOR PROTEIN; REGULATORY T-CELLS;
D O I
10.1146/annurev-pathol-012615-044231
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Sites of inflammation are defined by significant changes in metabolic activity. Recent studies have suggested that O-2 metabolism and hypoxia play a prominent role in inflammation so-called "inflammatory hypoxia," which results from a combination of recruited inflammatory cells (e.g., neutrophils and monocytes), the local proliferation of multiple cell types, and the activation of multiple O-2-consuming enzymes during inflammation. These shifts in energy supply and demand result in localized regions of hypoxia and have revealed the important function off the transcription factor HIF (hypoxia-inducible factor) in the regulation of key target genes that promote inflammatory resolution. Analysis of these pathways has provided multiple opportunities for understanding basic mechanisms of inflammation and has defined new targets for intervention. Here, we review recent work addressing tissue hypoxia and metabolic control of inflammation and immunity.
引用
收藏
页码:77 / 100
页数:24
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