Effect of Interleukin-8 and Monocyte Chemotactic Protein-1 on Adhesion of Circulating Granulocytes and Monocytes from Asthma Patients to Human Venous Endothelial Cells
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作者:
Els M. E. Verdegaal
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机构:University Hospital,Department of Infectious Diseases
Els M. E. Verdegaal
Suzanne T. Zegveld
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机构:University Hospital,Department of Infectious Diseases
Suzanne T. Zegveld
Henry Beekhuizen
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机构:University Hospital,Department of Infectious Diseases
Henry Beekhuizen
Wim Bakker
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机构:University Hospital,Department of Infectious Diseases
Wim Bakker
Ralph Van Furth
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机构:University Hospital,Department of Infectious Diseases
Ralph Van Furth
机构:
[1] University Hospital,Department of Infectious Diseases
[2] University Hospital Leiden.,Department of Clinical Oncology
Public Health;
Endothelial Cell;
Asthma;
Internal Medicine;
Inflammatory Response;
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摘要:
The adhesive interactions between phagocytes and endothelial cells (EC) can be modulated by inflammatory cytokines and chemotactic proteins which are released during an inflammatory response. The aim of the present study was to investigate first whether the adhesive properties of granulocytes and monocytes from asthma patients for vascular endothelial cells differ from those of phagocytes from healthy individuals. Furthermore, we studied whether the chemokines interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) can affect the binding of phagocytes to EC. No differences were observed in binding of phagocytes from asymptomatic or symptomatic asthma patients and from healthy individuals to non-stimulated or cytokine-stimulated EC. Incubation of granulocytes with IL-8 did not influence their adhesion to non-stimulated EC but inhibited the adhesion of granulocytes to IL-1-stimulated EC. Incubation of monocytes with MCP-1 did not affect their adhesion to non-stimulated or cytokine-stimulated EC. Our results indicate that adhesion of phagocytes to EC depends on the activation state of the endothelial cells but not on the origin of the phagocytes, since there were no differences in the adhesion of phagocytes from asthma patients and healthy individuals to non-stimulated or cytokine-stimulated EC.