Regulation of neutrophil function by adenosine

Kathryn E. Barletta, Klaus Ley, Borna Mehrad

Research output: Contribution to journalArticlepeer-review

174 Scopus citations


Adenosine is an endogenously released purine nucleoside that signals via 4 widely expressed G protein-coupled receptors: A 1, A 2A, A 2B, and A3. In the setting of inflammation, the generation and release of adenosine is greatly enhanced. Neutrophils play an important role in host defense against invading pathogens and are the cellular hallmark of acute inflammation. Neutrophils both release adenosine and can respond to it via expression of all 4 adenosine receptor subtypes. At low concentrations, adenosine can act via the A 1 and A 3 adenosine receptor subtypes to promote neutrophil chemotaxis and phagocytosis. At higher concentrations, adenosine acts at the lower-affinity A 2A and A 2B receptors to inhibit neutrophil trafficking and effector functions such as oxidative burst, inflammatory mediator production, and granule release. Modulation of neutrophil function by adenosine is relevant in a broad array of disease models, including ischemia reperfusion injury, sepsis, and noninfectious acute lung injury. This review will summarize relevant research in order to provide a framework for understanding how adenosine directly regulates various elements of neutrophil function.

Original languageEnglish (US)
Pages (from-to)856-864
Number of pages9
JournalArteriosclerosis, thrombosis, and vascular biology
Issue number4
StatePublished - Apr 2012
Externally publishedYes


  • adhesion
  • blood cells
  • chemotaxis
  • cytokines
  • host defense

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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