Hypoxia and Mucosal Inflammation

Sean P. Colgan, Eric L. Campbell, Douglas J. Kominsky

Research output: Contribution to journalArticle

38 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)77-100
Number of pages24
JournalAnnual Review of Pathology: Mechanisms of Disease
Volume11
DOIs
Publication statusPublished - 23 May 2016
Externally publishedYes

Keywords

  • Colitis
  • Creatine
  • Epithelium
  • Inflammation
  • Metabolism
  • Mucosa
  • Murine model
  • Neutrophil
  • Nucleoside
  • Nucleotidase
  • Nucleotide
  • Phosphocreatine

ASJC Scopus subject areas

  • Medicine(all)
  • Plant Science

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