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.