Overproduction of monocyte derived tumor necrosis factor alpha, interleukin (IL) 6, IL-8 and increased neutrophil superoxide generation in Behcet's disease. A comparative study with familial Mediterranean fever and healthy subjects.

Authors: Mege, JL  Dilsen, N  Sanguedolce, V  Gul, A  Bongrand, P  Roux, H  Ocal, L  Inanc, M  Capo, C 
Citation: Mege JL, etal., J Rheumatol. 1993 Sep;20(9):1544-9.
Pubmed: (View Article at PubMed) PMID:8164212

OBJECTIVE: The etiopathogenesis of Behcet's disease (BD) has not yet been clarified but might involve immune dysfunction. As cytokines are involved in the regulation of immune responses and inflammatory reactions, we investigated whether they may play a role in the pathogenesis of BD. METHODS: We investigated spontaneous and lipopolysaccharide (LPS) stimulated production of tumor necrosis factor alpha (TNF alpha), interleukin (IL) 1, IL-6, IL-8 and granulocyte monocyte macrophage colony stimulating factor (GM-CSF) by peripheral blood monocytes from 21 patients with BD, 10 healthy controls and 10 patients with familial Mediterranean fever (FMF), another chronic inflammatory disease. We also studied superoxide generation and surface antigen expression by polymorphonuclear neutrophils (PMN). RESULTS: The spontaneous secretion of TNF alpha, IL-6 and IL-8 by monocytes was significantly increased in patients with active BD. The secretion of TNF alpha, IL-1, IL-6 and IL-8 was found to be in normal range in asymptomatic patients with FMF. The LPS stimulated production of TNF alpha, IL-6, IL-1 and IL-8 was significantly increased in patients with BD, without any correlation with BD activity. In vitro, PMN spontaneously generated significant amounts of superoxide 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.


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CRRD Object Information
CRRD ID: 7829752
Created: 2014-01-23
Species: All species
Last Modified: 2014-01-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.