Abstract
At physiological concentrations, adenosine can modulate a variety of biological activities by engaging specific surface receptors, termed A1 and A2, with different affinity for adenosine and its analogues.1 Engagement of A2 adenosine receptors induces an increase in cAMP level in several cells types, in contrast stimulation of A1 receptors causes an opposite effect.2 In neutrophils, adenosine and its analogues inhibit O2 − generation, phagocytosis and adherence by occupancy of specific A2 adenosine receptors, while occupancy of A1 adenosine receptors enhance chemotaxis, phagocytosis and adherence.3,7 In general, activation of leukocytes adenosine receptors reduces immune and inflammatory responses.8 Therefore, it may be suggested that release of adenosine is one mechanism by which normal cells protect themselves from activated neutrophils. In fact, while stimulated neutrophils normally control bacterial infection, they may also contribute to the pathology of several inflammatory diseases including some rheumatoid diseases and emphysema.
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Martini, C., Trincavelli, L., Fiorini, M., Nardi, M., Lucacchini, A., Bazzichi, L. (1998). Effect of FMLP Stimulation on [3H]-NECA Binding to Adenosine Receptors in Neutrophils Membranes. In: Griesmacher, A., Müller, M.M., Chiba, P. (eds) Purine and Pyrimidine Metabolism in Man IX. Advances in Experimental Medicine and Biology, vol 431. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5381-6_17
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DOI: https://doi.org/10.1007/978-1-4615-5381-6_17
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