Rheumatology: Current Research
Open Access

Deregulation of NF-κB signal transduction is involved in the Sj�gren�s syndrome inflammatory process

International Conference and Exhibition on Orthopedics & Rheumatology

August 13-15, 2012 Hilton Chicago/Northbrook, USA

Massimo Amore

Accepted Abstracts: Rheumatology & Orthopedics

Abstract :

Background: Chronic inflammatory diseases are caused by prolonged production of pro-inflammatory cytokines and many pro-inflammatory cytokines are involved in the inflammatory process of primary Sj�?¶grenâ�?�?s syndrome. The transcription factor nuclear factor-�?ºB (NF�?ºB) is related to the transcription of these pro-inflammatory cytokines. Therefore, NF�?ºB plays an important role in inflammatory diseases and in the development of autoimmunity. We analyzed the importance of I�?ºB�?± (inhibitor of �?ºB alpha) as NF-�?ºB signal transduction inhibitor in monocytes from Sj�?¶grenâ�?�?s syndrome (SS) patients versus healthy controls. Methods: Monocytes were obtained from the peripheral blood of 30 SS patients and 23 healthy subjects. I�?ºB�?± expression was studied by semi quantitative RT-PCR, Real-Time PCR, immunoblotting, flow cytometry and ELISA. Results: Analysis of the gene and protein expression profiles of SS monocytes revealed a down-regulation of I�?ºB�?± and, all the Sj�?¶grenâ�?�?s syndrome cases examined, serum I�?ºB�?± levels were significantly decreased in comparison with controls. Conclusions: our findings clearly demonstrate changes in the levels of I�?ºB�?± in SS monocytes, suggesting that the attenuated expression of I�?ºB�?± could contribute to the deregulation of NF-�?ºB pathways in the SS pathogenesis. Decreased expression of I�?ºB�?± may specifically amplify cytokines production and inflammatory response linked to Sj�?¶grenâ�?�?s syndrome.