Adenosine: A potential mediator of immunosuppression in multiple organ failure

György Haskó, Edwin A. Deitch, Csaba Szabó, Zoltán H. Németh, E. Sylvester Vizi

    Research output: Contribution to journalReview articlepeer-review

    58 Scopus citations


    Multiple organ failure following a variety of insults, including, trauma, shock and pancreatitis, is the cause of 50-80% of all deaths in surgical intensive care units. In most patients, infections secondary to a general immunosuppressive state serve to trigger the development of multiple organ failure. This immunosuppressive state may be a consequence of excessive release of adenosine into the extracellular space, as adenosine has multiple immunosuppressive effects. Activation of adenosine receptors on immune cells inhibits the production of proinflammatory cytokines such as tumor necrosis factor α and interleukin (IL)-12, and increases the production of the anti-inflammatory cytokine IL-10. In addition, adenosine receptor activation appears to suppress cellular immunity by decreasing T helper cell (Th)1 and increasing Th2 responses. A deeper understanding of the role of adenosine in multiple organ failure may facilitate the development of adenosine-based therapeutic strategies.

    Original languageEnglish (US)
    Pages (from-to)440-444
    Number of pages5
    JournalCurrent Opinion in Pharmacology
    Issue number4
    StatePublished - Aug 1 2002

    ASJC Scopus subject areas

    • Pharmacology
    • Drug Discovery


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