OVERPRODUCTION OF MONOCYTE-DERIVED TUMOR-NECROSIS-FACTOR-ALPHA, INTERLEUKIN-(IL)-6, IL-8 AND INCREASED NEUTROPHIL SUPEROXIDE GENERATION IN BEHCETS-DISEASE - A COMPARATIVE-STUDY WITH FAMILIAL MEDITERRANEAN FEVER AND HEALTHY-SUBJECTS

Citation
Jl. Mege et al., OVERPRODUCTION OF MONOCYTE-DERIVED TUMOR-NECROSIS-FACTOR-ALPHA, INTERLEUKIN-(IL)-6, IL-8 AND INCREASED NEUTROPHIL SUPEROXIDE GENERATION IN BEHCETS-DISEASE - A COMPARATIVE-STUDY WITH FAMILIAL MEDITERRANEAN FEVER AND HEALTHY-SUBJECTS, Journal of rheumatology, 20(9), 1993, pp. 1544-1549
Citations number
44
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
0315162X
Volume
20
Issue
9
Year of publication
1993
Pages
1544 - 1549
Database
ISI
SICI code
0315-162X(1993)20:9<1544:OOMTI>2.0.ZU;2-M
Abstract
Objective. The etiopathogenesis of Behcet's disease (BD) has not yet b een clarified but might involve immune dysfunction. As cytokines are i nvolved in the regulation of immune responses and inflammatory reactio ns, we investigated whether they may play a role in the pathogenesis o f BD. Methods. We investigated spontaneous and lipopolysaccharide (LPS ) stimulated production of tumor necrosis factor alpha (TNFalpha), int erleukin (IL) 1, IL-6, IL-8 and granulocyte monocyte macrophage colony stimulating factor (GM-CSF) by peripheral blood monocytes from 21 pat ients with BD, 10 healthy controls and 10 patients with familial Medit erranean fever (FMF), another chronic inflammatory disease. We also st udied superoxide generation and surface antigen expression by polymorp honuclear neutrophils (PMN). Results. The spontaneous secretion of TNF alpha, IL-6 and IL-8 by monocytes was significantly increased in patie nts with active BD. The secretion of TNFalpha, IL-1, IL-6 and IL-8 was found to be in normal range in asymptomatic patients with FMF. The LP S stimulated production of TNFalpha, IL-6, IL-1 and IL-8 was significa ntly increased in patients with BD, without any correlation with BD ac tivity. In vitro, PMN spontaneously generated significant amounts of s uperoxide in patients with active BD. Conclusion. Taken together, our results suggest that monocyte and PMN dysfunctions may play a role in the pathogenesis of BD.