Inhibition of fMLP-triggered respiratory burst of human monocytes by adenosine: involvement of A3 adenosine receptor

Broussas, Matthieu; Cornillet‐Lefèbvre, Pascale; Potron, G; Nguyên, Philippe

doi:10.1002/jlb.66.3.495

Cited by 48 publications

(38 citation statements)

References 39 publications

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“…This is in line with data from other reports in which the inhibitory action of adenosine on ROI production and other biological answers in monocytes have been described (3,4,17,26,40). According to our data, the IC 50 s may result from a rapid uptake and an extensive metabolism of adenosine.…”

Section: Discussionsupporting

confidence: 93%

“…A previous study by Broussas et al (4) While Sullivan et al (42) suggested an involvement of cAMP in A 2 receptor-mediated regulation of the oxidative burst in human neutrophils, other groups have questioned an enhancement of cAMP as an effector mechanism in these cells (6,7). Alternative signal transduction mechanisms such as activation of a serine/threonine protein phosphatase (39) or participation of inositol 1,4,5-phosphate (IP3) in A 2 receptor-mediated events (34) have been proposed.…”

Section: Fig 7 (A)mentioning

confidence: 89%

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Regulation of Adenosine Receptor Subtypes during Cultivation of Human Monocytes: Role of Receptors in Preventing Lipopolysaccharide-Triggered Respiratory Burst

Thiele¹,

Kronstein²,

Wetzel³

et al. 2004

Infect Immun

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Section: Discussionsupporting

confidence: 93%

Section: Fig 7 (A)mentioning

confidence: 89%

Regulation of Adenosine Receptor Subtypes during Cultivation of Human Monocytes: Role of Receptors in Preventing Lipopolysaccharide-Triggered Respiratory Burst

Thiele¹,

Kronstein²,

Wetzel³

et al. 2004

Infect Immun

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“…mRNA for all 4 adenosine receptor subtypes was expressed in freshly isolated monocytes, and while the expression of A 1 , A 2B , and A 3 receptors did not vary during a 7-day cultivation period, the mRNA for A 2A receptors was up-regulated after day 1 and disappeared by day 7 of culture (Thiele et al, 2004). In agreement with the pharmacological data that IB-MECA was more potent than CGS 21680, an agonist which elicits its cellular effects mainly by activating the cAMP-PKA pathway (Lupica et al, 1990), the cAMP-dependent protein kinase inhibitor KT5720 failed to reverse the inhibitory effect of adenosine on fMLP-induced monocyte respiratory burst (Broussas et al, 1999). The inhibitory effect of adenosine on human monocyte/macrophage respiratory burst was recapitulated using both mouse (Si et al, 1997) and rat (Edwards et al, 1994) peritoneal macrophages; however, there was no detailed analysis of the adenosine receptors involved in either study.…”

Section: Adenosine Inhibits Monocyte/macrophage Oxidative Burstsupporting

confidence: 74%

“…Since adenosine did not decrease the PMA-induced respiratory burst, it was proposed that the mode of action of adenosine was not related to a direct effect on protein kinase C (PKC). Two later studies, one using fMLP (Broussas et al, 1999) and the other LPS (Thiele et al, 2004) to stimulate oxidative burst, confirmed that the effect of adenosine could be attributed primarily to A 3 receptor stimulation. This idea was supported by the observations that the A 3 receptor agonist N 6 -(3-iodobenzyl)-adenosine-5′-N-methyluronamide (IB-MECA) was more potent than the A 2A agonist CGS 21680 or A 1 receptor agonist R-PIA.…”

Section: Adenosine Inhibits Monocyte/macrophage Oxidative Burstmentioning

confidence: 89%

Shaping of monocyte and macrophage function by adenosine receptors

Haskó

Pacher

Deitch

et al. 2007

Pharmacology & Therapeutics

196

154

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Adenosine is an endogenous purine nucleoside that, following its release into the extracellular space, binds to specific adenosine receptors expressed on the cell surface. Adenosine appears in the extracellular space under metabolically stressful conditions, which are associated with ischemia, inflammation, and cell damage. There are 4 types of adenosine receptors (A 1 , A 2A , A 2B and A 3 ) and all adenosine receptors are members of the G protein-coupled family of receptors. Adenosine receptors are expressed on monocytes and macrophages and through these receptors adenosine modulates monocyte and macrophage function. Since monocytes and macrophages are activated by the same danger signals that cause accumulation of extracellular adenosine, adenosine receptors expressed on macrophages represent a sensor system that provide monocytes and macrophages with information about the stressful environment. Adenosine receptors, thus, allow monocytes and macrophages to fine-tune their responses to stressful stimuli. Here, we review the consequences of adenosine receptor activation on monocyte/macrophage function. We will detail the effect of stimulating the various adenosine receptor subtypes on macrophage differentiation/proliferation, phagocytosis, and tissue factor (TF) expression. We will also summarize our knowledge of how adenosine impacts the production of extracellular mediators secreted by monocytes and macrophages in response to toll-like receptor (TLR) ligands and other inflammatory stimuli. Specifically, we will delineate how adenosine affects the production of superoxide, nitric oxide (NO), tumor necrosis factor-α, interleukin (IL)-12, IL-10, and vascular endothelial growth factor (VEGF). A deeper insight into the regulation of monocyte and macrophage function by adenosine receptors should assist in developing new therapies for inflammatory diseases.

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“…LPS-induced oxidative burst of human neutrophils was determined as previously described (36). Briefly, PMNs of healthy volunteers were preincubated with luminol (50 mmol/ml) and stimulated with LPS in presence or absence of 29Me-CCPA (1 ng/ml).…”

Section: Oxidative Burst Of Human Neutrophilsmentioning

confidence: 99%

Adenosine Receptor A1 Regulates Polymorphonuclear Cell Trafficking and Microvascular Permeability in Lipopolysaccharide-Induced Lung Injury

Ngamsri

Wagner

Vollmer

et al. 2010

The Journal of Immunology

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Extracellular adenosine and adenosine receptors are critically involved in various inflammatory pathways. Adenosine receptor A1 (A1AR) has been implicated in mediating transmigration of leukocytes to sites of inflammation. This study was designed to characterize the role of A1AR in a murine model of LPS-induced lung injury. LPS-induced transmigration of polymorphonuclear cells (PMNs) and microvascular permeability was elevated in A1AR−/− mice. Pretreatment of wild-type mice with the specific A1AR agonist 2′Me–2-chloro-N6-cyclopentyladenosine attenuated PMN accumulation in the interstitium and alveolar space as well as microvascular permeability. Lower PMN counts in the lungs of pretreated wild-type mice were associated with reduced amounts of the chemotactic cytokines TNF-α, IL-6, and CXCL2/3 in the bronchoalveolar lavage. Pretreatment was only effective when A1AR was expressed on hematopoietic cells as demonstrated in chimeric mice. These findings were confirmed by in vitro transmigration assays demonstrating that chemokine-induced transmigration of PMNs was reduced when PMNs but not when pulmonary endothelial or alveolar epithelial cells were pretreated. 2′Me–2-chloro-N6-cyclopentyladenosine prevented pulmonary endothelial but not epithelial cells from LPS-induced cellular remodeling and cell retraction. Our data reveal what we believe to be a previously unrecognized distinct role of A1AR for PMN trafficking and endothelial integrity in a model of acute lung injury.

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Inhibition of fMLP-triggered respiratory burst of human monocytes by adenosine: involvement of A3 adenosine receptor

Cited by 48 publications

References 39 publications

Regulation of Adenosine Receptor Subtypes during Cultivation of Human Monocytes: Role of Receptors in Preventing Lipopolysaccharide-Triggered Respiratory Burst

Regulation of Adenosine Receptor Subtypes during Cultivation of Human Monocytes: Role of Receptors in Preventing Lipopolysaccharide-Triggered Respiratory Burst

Shaping of monocyte and macrophage function by adenosine receptors

Adenosine Receptor A1 Regulates Polymorphonuclear Cell Trafficking and Microvascular Permeability in Lipopolysaccharide-Induced Lung Injury

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