Dopamine attenuates the chemoattractant effect of interleukin-8: a novel role in the systemic inflammatory response syndrome.

Hdl Handle:
http://hdl.handle.net/10147/209105
Title:
Dopamine attenuates the chemoattractant effect of interleukin-8: a novel role in the systemic inflammatory response syndrome.
Authors:
Sookhai, S; Wang, J H; Winter, D; Power, C; Kirwan, W; Redmond, H P
Affiliation:
Department of Academic Surgery, Cork University Hospital and University College, Cork, Ireland.
Citation:
Shock. 2000 Sep;14(3):295-9.
Journal:
Shock (Augusta, Ga.)
Issue Date:
3-Feb-2012
URI:
http://hdl.handle.net/10147/209105
PubMed ID:
11028546
Abstract:
Activated neutrophil (PMN) adherence to vascular endothelium comprises a key step for both transendothelial migration and initiation of potentially deleterious release of PMN products. The biogenic amine, dopamine (DA), has been used for several decades in patients to maintain hemodynamic stability. The effect of dopamine on PMN transendothelial migration and adhesion receptor expression and on the endothelial molecules, E-selectin and ICAM-1, was evaluated. PMN were isolated from healthy controls, stimulated with lipopolysaccharide (LPS), and tumor necrosis factor-alpha (TNF-alpha) and treated with dopamine. CD 11b and CD 18 PMN adhesion receptor expression were assessed flow cytometrically. In a separate experiment, the chemoattractant peptide, IL-8, was placed in the lower chamber of transwells, and PMN migration was assessed. Human umbilical vein endothelial cells (HUVEC) were stimulated with LPS/TNF-alpha and incubated with dopamine. ICAM-1 and E-selectin endothelial molecule expression were assessed flow cytometrically. There was a significant increase in transendothelial migration in stimulated PMN compared with normal PMN (40 vs. 14%, P < 0.001). In addition, PMN CD11b/CD18 was significantly upregulated in stimulated PMN compared with normal PMN (252.4/352.4 vs. 76.7/139.4, P < 0.001) as were endothelial E-selectin/ICAM-1 expression compared with normal EC (8.1/9 vs. 3.9/3.8, P < 0.05). After treatment with dopamine, PMN transmigration was significantly decreased compared with stimulated PMN (8% vs. 40%, P < 0.001). Furthermore, dopamine also attenuated PMN CD11b/CD18 and the endothelial molecules E-selectin and ICAM-1 compared with stimulated PMN/EC that were not treated dopamine (174/240 vs. 252/352, P < 0.05 and 4/4.4 vs. 8.1/9, P < 0.05. respectively). The chemoattractant effect of IL-8 was also attenuated. These results identify for the first time that dopamine attenuates the initial interaction between PMN and the endothelium, and consequently, modulates PMN exudation. Thus, biogenic amines, including dopamine, may function as anti-inflammatory cytokines.
Language:
eng
MeSH:
Antigens, CD18/drug effects/metabolism; Cardiotonic Agents/pharmacology; Cell Movement/drug effects; Cells, Cultured; Dopamine/administration & dosage/*pharmacology; Dose-Response Relationship, Drug; Endothelium, Vascular/cytology/drug effects; Humans; Intercellular Adhesion Molecule-1/drug effects/metabolism; Interleukin-8/*physiology; Lipopolysaccharides/pharmacology; Macrophage-1 Antigen/drug effects/metabolism; Neutrophils/cytology/*drug effects/metabolism; Systemic Inflammatory Response Syndrome/blood/*physiopathology; Tumor Necrosis Factor-alpha/pharmacology
ISSN:
1073-2322 (Print); 1073-2322 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorSookhai, Sen_GB
dc.contributor.authorWang, J Hen_GB
dc.contributor.authorWinter, Den_GB
dc.contributor.authorPower, Cen_GB
dc.contributor.authorKirwan, Wen_GB
dc.contributor.authorRedmond, H Pen_GB
dc.date.accessioned2012-02-03T15:12:25Z-
dc.date.available2012-02-03T15:12:25Z-
dc.date.issued2012-02-03T15:12:25Z-
dc.identifier.citationShock. 2000 Sep;14(3):295-9.en_GB
dc.identifier.issn1073-2322 (Print)en_GB
dc.identifier.issn1073-2322 (Linking)en_GB
dc.identifier.pmid11028546en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209105-
dc.description.abstractActivated neutrophil (PMN) adherence to vascular endothelium comprises a key step for both transendothelial migration and initiation of potentially deleterious release of PMN products. The biogenic amine, dopamine (DA), has been used for several decades in patients to maintain hemodynamic stability. The effect of dopamine on PMN transendothelial migration and adhesion receptor expression and on the endothelial molecules, E-selectin and ICAM-1, was evaluated. PMN were isolated from healthy controls, stimulated with lipopolysaccharide (LPS), and tumor necrosis factor-alpha (TNF-alpha) and treated with dopamine. CD 11b and CD 18 PMN adhesion receptor expression were assessed flow cytometrically. In a separate experiment, the chemoattractant peptide, IL-8, was placed in the lower chamber of transwells, and PMN migration was assessed. Human umbilical vein endothelial cells (HUVEC) were stimulated with LPS/TNF-alpha and incubated with dopamine. ICAM-1 and E-selectin endothelial molecule expression were assessed flow cytometrically. There was a significant increase in transendothelial migration in stimulated PMN compared with normal PMN (40 vs. 14%, P < 0.001). In addition, PMN CD11b/CD18 was significantly upregulated in stimulated PMN compared with normal PMN (252.4/352.4 vs. 76.7/139.4, P < 0.001) as were endothelial E-selectin/ICAM-1 expression compared with normal EC (8.1/9 vs. 3.9/3.8, P < 0.05). After treatment with dopamine, PMN transmigration was significantly decreased compared with stimulated PMN (8% vs. 40%, P < 0.001). Furthermore, dopamine also attenuated PMN CD11b/CD18 and the endothelial molecules E-selectin and ICAM-1 compared with stimulated PMN/EC that were not treated dopamine (174/240 vs. 252/352, P < 0.05 and 4/4.4 vs. 8.1/9, P < 0.05. respectively). The chemoattractant effect of IL-8 was also attenuated. These results identify for the first time that dopamine attenuates the initial interaction between PMN and the endothelium, and consequently, modulates PMN exudation. Thus, biogenic amines, including dopamine, may function as anti-inflammatory cytokines.en_GB
dc.language.isoengen_GB
dc.subject.meshAntigens, CD18/drug effects/metabolismen_GB
dc.subject.meshCardiotonic Agents/pharmacologyen_GB
dc.subject.meshCell Movement/drug effectsen_GB
dc.subject.meshCells, Cultureden_GB
dc.subject.meshDopamine/administration & dosage/*pharmacologyen_GB
dc.subject.meshDose-Response Relationship, Drugen_GB
dc.subject.meshEndothelium, Vascular/cytology/drug effectsen_GB
dc.subject.meshHumansen_GB
dc.subject.meshIntercellular Adhesion Molecule-1/drug effects/metabolismen_GB
dc.subject.meshInterleukin-8/*physiologyen_GB
dc.subject.meshLipopolysaccharides/pharmacologyen_GB
dc.subject.meshMacrophage-1 Antigen/drug effects/metabolismen_GB
dc.subject.meshNeutrophils/cytology/*drug effects/metabolismen_GB
dc.subject.meshSystemic Inflammatory Response Syndrome/blood/*physiopathologyen_GB
dc.subject.meshTumor Necrosis Factor-alpha/pharmacologyen_GB
dc.titleDopamine attenuates the chemoattractant effect of interleukin-8: a novel role in the systemic inflammatory response syndrome.en_GB
dc.contributor.departmentDepartment of Academic Surgery, Cork University Hospital and University College, Cork, Ireland.en_GB
dc.identifier.journalShock (Augusta, Ga.)en_GB
dc.description.provinceMunster-
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