Differential expression of adenosine receptors in human neutrophils: up-regulation by specific Th1 cytokines and lipopolysaccharide

Fortin, Andrée; Harbour, Danielle; Fernandes, Maria J.; Borgeat, Pierre; Bourgoin, Sylvain G.

doi:10.1189/jlb.0505249

Cited by 57 publications

(60 citation statements)

References 55 publications

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“…From the point of view of the use of A 3 AR KO mice in this study, important findings are those showing that adenosine A 3 receptors are expressed in human neutrophils [18], monocytes [19], and lymphocytes [20], and especially in the differentiating and proliferating cells of various hematopoietic cell compartments, namely in mouse bone marrow granulopoietic/ monocytopoietic, erythropoietic, and B-lymphopoietic cells, as well as in the T-lymphopoietic cells of the thymus [21]. Thus, the lack of these receptors in A 3 AR KO mice could be expected to be connected with modulation and/or disorders of hematopoiesis.…”

Section: Discussionmentioning

confidence: 99%

Lack of adenosine A3 receptors causes defects in mouse peripheral blood parameters

Höfer

Pospı́šil

Dušek

et al. 2014

Purinergic Signalling

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The role of the adenosine A 3 receptor in hematopoiesis was studied using adenosine A 3 receptor knockout (A 3 AR KO) mice. Hematological parameters of peripheral blood and femoral bone marrow of irradiated and untreated A 3 AR KO mice and their wild-type (WT) counterparts were investigated. Irradiation of the mice served as a defined hematopoiesis-damaging means enabling us to evaluate contingent differences in the pattern of experimentally induced hematopoietic suppression between the A 3 AR KO mice and WT mice. Defects were observed in the counts and/or functional parameters of blood cells in the A 3 AR KO mice. These defects include statistically significantly lower values of blood neutrophil and monocyte counts, as well as those of mean erythrocyte volume, mean erythrocyte hemoglobin, blood platelet counts, mean platelet volume, and plateletcrit, and can be considered to bear evidence of the lack of a positive role played by the adenosine A 3 receptor in the hematopoietic system. Statistically significantly increased values of the bone marrow parameters studied in A 3 AR KO mice (femoral bone marrow cellularity, granulocyte/macrophage progenitor cells, and erythrocyte progenitor cells) can probably be explained by compensatory mechanisms attempting to offset the disorders in the function of blood elements in these mice. The pattern of the radiation-induced hematopoietic suppression was very similar in A 3 AR KO mice and their WT counterparts.

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Section: Discussionmentioning

confidence: 99%

Lack of adenosine A3 receptors causes defects in mouse peripheral blood parameters

Höfer

Pospı́šil

Dušek

et al. 2014

Purinergic Signalling

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“…All inhibitory effects of adenosine on neutrophil functions are mediated by A 2A receptors [49], which increase intracellular cAMP levels and decrease the proinflammatory action of PMNs [50]. In an important way, the activation of this receptor subtype occurs when the nucleoside is found in high concentrations.…”

Section: Discussionmentioning

confidence: 99%

Involvement of purinergic signaling on nitric oxide production by neutrophils stimulated with Trichomonas vaginalis

Frasson

Carli

Bonan

et al. 2011

Purinergic Signalling

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Trichomonas vaginalis is a parasite from the human urogenital tract that causes trichomonosis, the most prevalent non-viral sexually transmitted disease. The neutrophil infiltration has been considered to be primarily responsible for cytological changes observed at infection site, and the chemoattractants can play an important role in this leukocytic recruitment. Nitric oxide (NO) is one of the most widespread mediator compounds, and it is implicated in modulation of immunological mechanisms. Extracellular nucleotides and nucleosides are signaling molecules involved in several processes, including immune responses and control of leukocyte trafficking. Ectonucleoside triphosphate diphosphohydrolase members, ecto-5′-nucleotidase, and adenosine deaminase (ectoADA) have been characterized in T. vaginalis. Herein, we investigated the effects of purinergic system on NO production by neutrophils stimulated with T. vaginalis. The trophozoites were able to induce a high NO synthesis by neutrophils through iNOS pathway. The extracellular nucleotides ATP, ADP, and ATPγS (a nonhydrolyzable ATP analog) showed no significant change in NO secretion. In contrast, adenosine and its degradation product, inosine, promoted a low production of the compound. The immunosuppressive effect of adenosine upon NO release by neutrophils occurred due to adenosine A 2A receptor activation. The ecto-5′-nucleotidase activity displayed by T. vaginalis was shown to be important in adenosine generation, indicating the efficiency of purinergic cascade. Our data suggest the influence of purinergic signaling, specifically adenosinergic system, on NO production by neutrophils in T. vaginalis infection, contributing to the immunological aspects of disease.

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“…A couple of recent studies have demonstrated that mechanical ventilation in rats and mice increases the level of pulmonary adenosine (13,14), and that mice deficient for extracellular adenosine generation show increased pulmonary edema and inflammation after VILI (14). Once in the extracellular milieu, adenosine exerts its biological effects through binding to the G-protein coupled adenosine receptors including A 1 R, A 2A R, A 2B R, and A 3 R (8,15,16). The A 2A R expressed on leukocytes and lung displays high affinity for adenosine (8).…”

Section: Introductionmentioning

confidence: 99%

Protective effects of adenosine A2A receptor agonist in ventilator-induced lung injury in rats

Chen

Peñuelas

Quinn

et al. 2009

Critical Care Medicine

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Objectives-Mechanical ventilation is associated with overwhelming inflammatory responses that are associated with ventilator-induced lung injury (VILI) in patients with acute respiratory distress syndrome. The activation of adenosine A 2A receptors has been reported to attenuate inflammatory cascades. Hypothesis-The administration of A 2A receptors agonist ameliorates VILI.Methods-Rats were subjected to hemorrhagic shock and resuscitation as a first hit to induce systemic inflammation. The animals randomly received the selective A 2A receptor agonist CGS-21680 or a vehicle control in a blinded fashion at the onset of resuscitation phase. They were then randomized to receive mechanical ventilation as a second hit with a high tidal volume of 20 mL/kg and zero positive end-expiratory pressure, or a low tidal volume of 6 mL/kg with positive end-expiratory pressure of 5 cm H 2 O.Results-The administration of CGS-21680 attenuated lung injury as evidenced by a decrease in respiratory elastance, lung edema, lung injury scores, neutrophil recruitment in the lung, and production of inflammatory cytokines, compared with the vehicle treated animals.Conclusions-The selective A 2A receptor agonist may have a place as a novel therapeutic approach in reducing VILI.

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Differential expression of adenosine receptors in human neutrophils: up-regulation by specific Th1 cytokines and lipopolysaccharide

Cited by 57 publications

References 55 publications

Lack of adenosine A3 receptors causes defects in mouse peripheral blood parameters

Lack of adenosine A3 receptors causes defects in mouse peripheral blood parameters

Involvement of purinergic signaling on nitric oxide production by neutrophils stimulated with Trichomonas vaginalis

Protective effects of adenosine A2A receptor agonist in ventilator-induced lung injury in rats

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