title: Hypoxia and Mucosal Inflammation.
abstract: Sites of inflammation are defined by significant changes in metabolic activity. Recent studies have suggested that O2 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 O2-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.
authors.affiliation: Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado 80045; email: sean.colgan@ucdenver.edu.|Mucosal Inflammation Program, University of Colorado School of Medicine, Aurora, Colorado 80045.
authors.forename: Sean P
authors.initials: SP
authors.lastname: Colgan
authors.affiliation: Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado 80045; email: sean.colgan@ucdenver.edu.|Mucosal Inflammation Program, University of Colorado School of Medicine, Aurora, Colorado 80045.
authors.forename: Eric L
authors.initials: EL
authors.lastname: Campbell
authors.affiliation: Mucosal Inflammation Program, University of Colorado School of Medicine, Aurora, Colorado 80045.|Department of Microbiology and Immunology, Montana State University, Bozeman, Montana 59717.
authors.forename: Douglas J
authors.initials: DJ
authors.lastname: Kominsky
mesh_terms: D000818:Animals; D006801:Humans; D000860:Hypoxia / Q000150:complications / Q000503:physiopathology*; D007249:Inflammation / Q000503:physiopathology*; D052016:Mucositis / Q000209:etiology* / Q000473:pathology; D009092:Mucous Membrane / Q000473:pathology*
keywords: colitis; creatine; epithelium; inflammation; metabolism; mucosa; murine model; neutrophil; nucleoside; nucleotidase; nucleotide; phosphocreatine