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Hypoxia, the HIF pathway and neutrophilic inflammatory responses

Research output: Contribution to journalLiterature reviewpeer-review

Original languageEnglish
Pages (from-to)471-477
Number of pages7
JournalBiological Chemistry
Issue number4
Publication statusPublished - Apr 2013


Many inflammatory diseases are characterised by persistent and inappropriate neutrophil activation, systemic or localised hypoxia, and bacterial colonisation. Hypoxia represents an important regulator of inflammatory responses because it inhibits neutrophil apoptosis, a process central to the timely resolution of inflammation. Progress in understanding how cells respond to hypoxia has led to the identification of hypoxia-inducible transcription factors (HIFs) and their hydroxylation by the prolyl hydroxylase enzymes. There is now a significant body of data to support a critical role for this HIF pathway in regulating neutrophil function. Moreover, manipulations of specific components of this pathway have very divergent effects on myeloid cell function. In this review, we will discuss the role individual members of the HIF pathway play in regulating key neutrophil functions and the implications this has for the development of effective therapeutic strategies that selectively target inappropriate neutrophil persistence while maintaining a fully competent immune response.

    Research areas

  • innate immunity, myeloid cell, oxygen sensing, prolyl hydroxylase domain-containing enzymes (PHDs), NF-KAPPA-B, INDUCIBLE-FACTOR, OXYGEN SENSOR, APOPTOSIS, HIF-1-ALPHA, ACTIVATION, RESOLUTION, MIGRATION, SEPSIS, PHD3

ID: 17164302