STUDY OF EOSINOPHIL-ENDOTHELIAL ADHESION, PRODUCTION OF OXYGEN RADICALS AND RELEASE OF EOSINOPHIL CATIONIC PROTEIN BY PERIPHERAL-BLOOD EOSINOPHILS OF PATIENTS WITH RHEUMATOID-ARTHRITIS

Citation
Av. Mertens et al., STUDY OF EOSINOPHIL-ENDOTHELIAL ADHESION, PRODUCTION OF OXYGEN RADICALS AND RELEASE OF EOSINOPHIL CATIONIC PROTEIN BY PERIPHERAL-BLOOD EOSINOPHILS OF PATIENTS WITH RHEUMATOID-ARTHRITIS, Clinical and experimental allergy, 23(10), 1993, pp. 868-873
Citations number
26
Categorie Soggetti
Allergy,Immunology
ISSN journal
09547894
Volume
23
Issue
10
Year of publication
1993
Pages
868 - 873
Database
ISI
SICI code
0954-7894(1993)23:10<868:SOEAPO>2.0.ZU;2-O
Abstract
Beside lymphocytes and neutrophils, eosinophils are also involved in t he inflammatory reaction in rheumatoid arthritis (RA). In this study, adhesion characteristics of peripheral blood eosinophils were studied in 43 RA patients and 19 controls, together with the expression of the beta2-integrin Mac-1 (CD11b/CD18). In addition, the production of oxy gen radicals of isolated peripheral blood eosinophils and serum levels of eosinophil cationic protein (ECP) were measured in order to evalua te eosinophil activation. Adhesion of eosinophils to unstimulated huma n vascular endothelium was significantly higher in RA patients with ac tive disease (n = 4) compared with controls (n = 14) (P<0.005) and com pared with patients with less active RA (n = 16) (P<0.05). Nevertheles s, the expression of the adhesion molecule Mac-1 (CD11b/CD18) was not increased in RA patients. ECP levels were higher in RA patients with a ctive disease (P<0.01). Release of oxygen radicals in response to phor bol stimulation was significantly elevated in active RA compared with controls (P<0.05) and to less active RA (P<0.05). We conclude that eos inophils of RA patients, especially those with active disease, are act ivated or at least primed and are involved in the inflammatory process in RA, analogous to the inflammation in asthma. The higher adhesion t o inflamed endothelium is indicative of a higher infiltration in the j oints, where tissue damage can be caused by toxic oxygen radicals and by granular proteins, such as ECP.