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The role of plasma adenosine deaminase in chemoattractant-stimulated oxygen radical production in neutrophils
Örebro universitet, Hälsoakademin. Fac Hlth Sci, Dept Med & Hlth Sci, Div Cardiovasc Med, Linköping Univ, Linköping, Sweden.
Fac Hlth Sci, Dept Med & Hlth Sci, Div Drug Res, Linköping Univ, Linköping, Sweden.
Örebro universitet, Hälsoakademin. Fac Hlth Sci, Dept Med & Hlth Sci, Div Drug Res, Linköping Univ, Linköping, Sweden.
2010 (engelsk)Inngår i: European Journal of Cell Biology, ISSN 0171-9335, E-ISSN 1618-1298, Vol. 89, nr 6, s. 462-467Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objectives: Adenosine deaminase (ADA) has a role in many immunity mediated disorders, such as asthma, tuberculosis and coronary artery disease. This study aims to investigate the ability of plasma ADA to modulate reactive oxygen species (ROS) production in neutrophils, and examine the involvement of adenosine and the cyclic AMP signaling pathway in this process. Methods: Neutrophils were stimulated, in the absence or presence of plasma, with the chemotactic peptide fMLP (formyl-methionyl-leucyl-phenylalanine), and the ROS production was determined with luminol-enhanced chemiluminescence. Activity of ADA was measured spectrophotometrically. Results: Plasma dose-dependently amplified the ROS generation in fMLP-stimulated neutrophils. In parallel, incubation of neutrophils in plasma elevated the total ADA-activity approximately 10 times from 1.3 U/ml to 12 U/ml. Inhibition of ADA, or type IV phosphodiesterases, significantly lowered the plasma-mediated ROS production. Furthermore, the high-affinity adenosine A(1) receptor antagonists DPCPX and 8-phenyltheophylline markedly inhibited the plasma-induced respiratory burst in neutrophils, suggesting an AI receptor-mediated mechanism. Conclusions: This study suggests that plasma ADA amplifies the release of toxic oxygen radicals from neutrophils through a downregulation of the inhibitory adenosine/cAMP-system and an enhanced activation of the stimulatory adenosine A(1)-receptor. This mechanism has probably a crucial role in regulating neutrophil function and in the defence against microbial infections. However, a sustained neutrophil activation could also contribute to inflammatory disorders such as atherosclerosis. (C) 2010 Elsevier GmbH. All rights reserved.

sted, utgiver, år, opplag, sider
2010. Vol. 89, nr 6, s. 462-467
Emneord [en]
Leukocyte, Reactive oxygen species, Adenosine deaminase, Plasma, Phosphodiesterase, Inflammation, Adenosine A1 receptor antagonist
HSV kategori
Forskningsprogram
Medicin
Identifikatorer
URN: urn:nbn:se:oru:diva-12959DOI: 10.1016/j.ejcb.2009.12.004ISI: 000277688100005OAI: oai:DiVA.org:oru-12959DiVA, id: diva2:383125
Tilgjengelig fra: 2011-01-04 Laget: 2011-01-03 Sist oppdatert: 2018-04-23bibliografisk kontrollert

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