Adenosine-A3 receptors in neutrophil microdomains promote the formation of bacteria-tethering cytonemes

Corriden, Ross and Self, Tim and Akong-Moore, Kathryn and Nizet, Victor and Kellam, Barrie and Briddon, Stephen J. and Hill, Stephen J. (2013) Adenosine-A3 receptors in neutrophil microdomains promote the formation of bacteria-tethering cytonemes. EMBO

The role of adenosine A3 receptors in cytotoxicity of the breast cancer cell lines

The nucleoside adenosine is present within cells and body fluids of all living organisms and its production, both intra- and extracellularly, is tightly coupled to energy consumption resulting in increased level of extracellular adenosine. The physiological effects of adenosine are mediated through four pharmacologically and biochemically distinct adenosine receptors (AR), i.e. A1, A2A, A2B and...

ATP release guides neutrophil chemotaxis via P2Y2 and A3 receptors.

Cells must amplify external signals to orient and migrate in chemotactic gradient fields. We find that human neutrophils release adenosine triphosphate (ATP) from the leading edge of the cell surface to amplify chemotactic signals and direct cell orientation by feedback through P2Y2 nucleotide receptors. Neutrophils rapidly hydrolyze released ATP to adenosine that then acts via A3-type adenosin...

Role of adenosine in response to vascular inflammation.

Adenosine is an endogenously released purine nucleoside that signals via 4 widely expressed G protein-coupled receptors: A1, A2A, A2B, 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 adeno...

A putative osmoreceptor system that controls neutrophil function through the release of ATP, its conversion to adenosine, and activation of A2 adenosine and P2 receptors.

We have previously shown that hypertonic stress (HS) can suppress chemoattractant-induced neutrophil responses via cyclic adenosine monophosphate and enhance these responses through p38 mitogen-activated protein kinase (MAPK) activation. The underlying mechanisms are unknown. Here, we report that HS dose-dependently releases adenosine 5'-triphosphate (ATP) from neutrophils and that extracellula...