Effects of adenosine on guinea pig pulmonary eosinophils

Walker, Blair

doi:10.1007/bf01487741

Cited by 11 publications

(6 citation statements)

References 39 publications

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“…However, the role of the A 3 R in eosinophil degranulation is controversial. In vitro studies have demonstrated that engagement of the A 3 R on guinea pig pulmonary eosinophils can induce superoxide production (26). In contrast, studies on cultured human peripheral blood eosinophils do not support a role for A 3 R engagement in stimulating eosinophil degranulation (43,44), and there is evidence that it may even prevent degranulation (25).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, there is evidence that A 3 R signaling can influence inflammatory cell functions relevant to pulmonary disease. For example, engagement of the A 3 R on mouse mast cells promotes mediator release (23,24), and engagement of the A 3 R on eosinophils exhibits both pro- (25) and antiinflammatory (20,21,26) activities. Similarly, there is evidence that A 3 R engagement can serve pro-and antiinflammatory roles on macrophages and neutrophils (27)(28)(29).…”

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confidence: 99%

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A₃Adenosine Receptor Signaling Influences Pulmonary Inflammation and Fibrosis

Morschl¹,

Molina²,

Volmer³

et al. 2008

Am J Respir Cell Mol Biol

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Adenosine is a signaling molecule produced during conditions that cause cellular stress or damage. This signaling pathway is implicated in the regulation of pulmonary disorders through the selective engagement of adenosine receptors. The goal of this study was to examine the involvement of the A 3 adenosine receptor (A 3 R) in a bleomycin model of pulmonary inflammation and fibrosis. Results demonstrated that A 3 R-deficient mice exhibit enhanced pulmonary inflammation that included an increase in eosinophils. Accordingly, there was a selective up-regulation of eosinophil-related chemokines and cytokines in the lungs of A 3 R-deficient mice exposed to bleomycin. This increase in eosinophil numbers was accompanied by a decrease in the amount of extracellular eosinophil peroxidase activity in lavage fluid from A 3 Rdeficient mice exposed to bleomycin, an observation suggesting that the A 3 R is necessary for eosinophil degranulation in this model. Despite an increase in inflammatory metrics associated with A 3 Rdeficient mice treated with bleomycin, there was little difference in the degree of pulmonary fibrosis. Examination of fibrotic mediators demonstrated enhanced transforming growth factor (TGF)-b1 expression, but not a concomitant increase in TGF-b1 activity. This was associated with the loss of expression of matrix metalloprotease 9, an activator of TGF-b1, in alveolar macrophages and airway mast cells in the lungs of A 3 R-deficient mice. Together, these results suggest that the A 3 R serves antiinflammatory functions in the bleomycin model, and is also involved in regulating the production of mediators that can impact fibrosis.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

A₃Adenosine Receptor Signaling Influences Pulmonary Inflammation and Fibrosis

Morschl¹,

Molina²,

Volmer³

et al. 2008

Am J Respir Cell Mol Biol

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“…However, the role of adenosine and A 3 receptor signalling on this cell type remains controversial with both pro- and anti-inflammatory activities of adenosine being reported. Adenosine was shown to potentiate the production of O 2 − by guinea pig pulmonary eosinophils [ 103 ]. However, an inhibition of degranulation and O 2 − anion release from human eosinophils was observed later and shown to be mediated by A 3 receptors [ 104 ].…”

Section: Purinergic Signalling In the Main Subsets Of Immune Cellsmentioning

confidence: 99%

Purinergic signalling and immune cells

Burnstock

Boeynaems

2014

Purinergic Signalling

254

222

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This review article provides a historical perspective on the role of purinergic signalling in the regulation of various subsets of immune cells from early discoveries to current understanding. It is now recognised that adenosine 5′-triphosphate (ATP) and other nucleotides are released from cells following stress or injury. They can act on virtually all subsets of immune cells through a spectrum of P2X ligand-gated ion channels and G protein-coupled P2Y receptors. Furthermore, ATP is rapidly degraded into adenosine by ectonucleotidases such as CD39 and CD73, and adenosine exerts additional regulatory effects through its own receptors. The resulting effect ranges from stimulation to tolerance depending on the amount and time courses of nucleotides released, and the balance between ATP and adenosine. This review identifies the various receptors involved in the different subsets of immune cells and their effects on the function of these cells.

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“…Aside from its potential role as a mediator of bronchoconstriction, adenosine may also modulate inflammation by its ability to regulate the activity of inflammatory cells [8,9]. In general, adenosine has an anti‐inflammatory effect on leucocytes [10]. Adenosine inhibits neutrophil granule release [11] and superoxide ion (O 2 − ) production [9].…”

Section: Introductionmentioning

confidence: 99%