
Vol. 113, No. 2, 2005
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Original Paper
Effect of Cytokines and Chemokines on Sickle Neutrophil Adhesion to Fibronectin
Angêla Assis, Nicola Conran, Andreia A. Canalli, Irene Lorand-Metze, Sara T.O. Saad, Fernando F. Costa
Haematology and Haemotherapy Centre, State University of Campinas, Campinas, UNICAMP, Brazil
Address of Corresponding Author
Acta Haematol 2005;113:130-136 (DOI: 10.1159/000083451)
Key Words
- Adhesion molecules
- Cytokines
- Leukocytes
- Sickle cell
Abstract
A role for leukocytes in sickle cell vaso-occlusive crisis is becoming increasingly recognized. Neutrophil counts are higher in sickle cell patients and neutrophils from these patients demonstrate increased adhesion to endothelial monolayers under certain circumstances. The effects of selected cytokines on the adhesion mechanisms of normal neutrophils and neutrophils from sickle cell anaemia patients (SCA neutrophils) were investigated. Neutrophils were separated from the blood of homozygous (HbSS) SCA patients and healthy controls. Following pre-incubation (25 min, 37°C) of the cells with cytokines, the adhesion of the cells to fibronectin (FN)-coated plates (20 µg/ml) was determined (60 min, 37°C, 5% CO2). Basal adhesion of normal and SCA neutrophils to FN was not statistically different. Pretreatment of normal neutrophils with either IL-6 (10-100 pg/ml), GCSF (1- 10 ng/ml) or IL-8 (1-100 ng/ml) had no significant effect upon their adhesion to FN. In contrast, SCA neutrophil adhesion to FN was increased significantly following pre-incubation with IL-6, G-CSF and IL-8 (p < 0.01). RANTES (1-100 ng/ml) had no significant effect on either normal or SCA neutrophil adhesion to FN. Flow-cytometric analyses demonstrated that IL-8 (10 ng/ml) significantly augments CD11b (Mac-1 integrin subunit) expression on SCA neutrophils, but not normal neutrophils. IL-6 and G-CSF (10 pg/ml and 10 ng/ml, respectively), however, had no effect on SCA neutrophil adhesion molecule expression. In conclusion, SCA neutrophil adhesion mechanisms may increase in the presence of certain cytokines, in vivo, and this activation may contribute to the physiopathology of sickle cell disease. Copyright © 2005 S. Karger AG, Basel
Author Contacts
Fernando F. Costa, MD, PhD Hemocentro, Rua Carlos Chagas, 480 Cidade Universitária, Barão Geraldo Campinas 13083-970-SP (Brazil) Tel. +55 19 3788 8734, Fax +55 19 3289 1089, E-Mail ferreira@unicamp.br
Article Information
Received: January 26, 2004
Accepted after revision: June 7, 2004
Number of Print Pages : 7
Number of Figures : 1, Number of Tables : 2, Number of References : 33 |
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