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    Dopamine induces neutrophil apoptosis through a dopamine D-1 receptor-independent mechanism.

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    Authors
    Sookhai, S
    Wang, J H
    McCourt, M
    O'Connell, D
    Redmond, H P
    Affiliation
    Department of Surgery, Cork University Hospital, Ireland.
    Issue Date
    2012-02-03T15:13:27Z
    MeSH
    Adult
    Aged
    Antigens, CD18/analysis
    Apoptosis/*drug effects
    Cytotoxicity, Immunologic/drug effects
    Dopamine/*pharmacology
    Humans
    Macrophage-1 Antigen/analysis
    Middle Aged
    Neutrophils/*drug effects/immunology
    Receptors, Dopamine D1/*physiology
    Systemic Inflammatory Response Syndrome/immunology
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    Metadata
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    Citation
    Surgery. 1999 Aug;126(2):314-22.
    Journal
    Surgery
    URI
    http://hdl.handle.net/10147/209145
    PubMed ID
    10455900
    Abstract
    BACKGROUND: For the normal resolution of an acute inflammatory response, neutrophil (PMN) apoptosis is essential to maintain immune homeostasis and to limit inappropriate host tissue damage. A delay in PMN apoptosis has been implicated in the pathogenesis of the systemic inflammatory response syndrome (SIRS). Dopamine, a biogenic amine with known cardiovascular and neurotransmitter properties, is used in patients with SIRS to maintain hemodynamic stability. We sought to determine whether dopamine may also have immunoregulatory properties capable of influencing PMN apoptosis, function, and activation state in patients with SIRS. METHODS: PMNs were isolated from healthy volunteers and patients with SIRS and treated with varying doses of dopamine and a dopamine D-1 receptor agonist, fenoldopam. PMN apoptosis was assessed every 6 hours with use of propidium iodide DNA staining and PMN function was assessed with use of respiratory burst activity, phagocytosis ability, and CD11a, CD11b, and CD18 receptor expression as functional markers. RESULTS: There was a significant delay in PMN apotosis in patients with SIRS compared with controls. Treatment of isolated PMNs from both healthy controls and patients with SIRS with 10 and 100 mumol/L dopamine induced apoptosis. PMN ingestive and cytocidal capacity were both decreased in patients with SIRS compared with controls. Treatment with dopamine significantly increased phagocytic function. Fenoldopam did not induce PMN apoptosis. CONCLUSION: Our data demonstrate for the first time that dopamine induces PMN apoptosis and modulates PMN function both in healthy controls and in patients with SIRS. These results indicate that dopamine may be beneficial during SIRS through a nonhemodynamic PMN-dependent proapoptotic mechanism.
    Language
    eng
    ISSN
    0039-6060 (Print)
    0039-6060 (Linking)
    Collections
    Cork University Hospital

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