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

Hdl Handle:
http://hdl.handle.net/10147/209145
Title:
Dopamine induces neutrophil apoptosis through a dopamine D-1 receptor-independent mechanism.
Authors:
Sookhai, S; Wang, J H; McCourt, M; O'Connell, D; Redmond, H P
Affiliation:
Department of Surgery, Cork University Hospital, Ireland.
Citation:
Surgery. 1999 Aug;126(2):314-22.
Journal:
Surgery
Issue Date:
3-Feb-2012
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
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
ISSN:
0039-6060 (Print); 0039-6060 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorSookhai, Sen_GB
dc.contributor.authorWang, J Hen_GB
dc.contributor.authorMcCourt, Men_GB
dc.contributor.authorO'Connell, Den_GB
dc.contributor.authorRedmond, H Pen_GB
dc.date.accessioned2012-02-03T15:13:27Z-
dc.date.available2012-02-03T15:13:27Z-
dc.date.issued2012-02-03T15:13:27Z-
dc.identifier.citationSurgery. 1999 Aug;126(2):314-22.en_GB
dc.identifier.issn0039-6060 (Print)en_GB
dc.identifier.issn0039-6060 (Linking)en_GB
dc.identifier.pmid10455900en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209145-
dc.description.abstractBACKGROUND: 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.en_GB
dc.language.isoengen_GB
dc.subject.meshAdulten_GB
dc.subject.meshAgeden_GB
dc.subject.meshAntigens, CD18/analysisen_GB
dc.subject.meshApoptosis/*drug effectsen_GB
dc.subject.meshCytotoxicity, Immunologic/drug effectsen_GB
dc.subject.meshDopamine/*pharmacologyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshMacrophage-1 Antigen/analysisen_GB
dc.subject.meshMiddle Ageden_GB
dc.subject.meshNeutrophils/*drug effects/immunologyen_GB
dc.subject.meshReceptors, Dopamine D1/*physiologyen_GB
dc.subject.meshSystemic Inflammatory Response Syndrome/immunologyen_GB
dc.titleDopamine induces neutrophil apoptosis through a dopamine D-1 receptor-independent mechanism.en_GB
dc.contributor.departmentDepartment of Surgery, Cork University Hospital, Ireland.en_GB
dc.identifier.journalSurgeryen_GB
dc.description.provinceMunster-

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