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Over expression of IL-32 in rheumatoid arthritis modulates NF-κB activity

 
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Research Article  
dx.doi.org/10.18081/2333-5106/015-12/793-811
American Journal of BioMedicine Volume 3, Issue 12, pages 793-811Received: April 02, 2015; accepted: November 22, 2015; published: December 25, 2015

Sergio Ayalaa, Peter G. Thurya,  Rui Chena, b, Jone A. Fishbeina, Maria Wisemana, Florian K. Dinulescua mail of corresponding author

Abstract

IL-32 is pro-inflammatory cytokine characterized by the induction of nuclear factor NF-κB activation and an important role in key cellular processes related to inflammation. We investigated whether the IL-32 expression may be involved in the mehanistic of rheumatoid arthritis through modulates the activity of NF-κB. We report that the concentrations of IL-32 are higher in the serums of RA patients than of control subjects. Results show that IL-32 induces the production of the proinflammatory cytokines IL-1-beta, IL-6, and increased NF-κB activation. We concluded that these data show that IL-32 is constitutively produced by RA synoviocytes, induces proinflammatory cytokine secretion, and activation NF-κB. IL-32 thereby may constitute a promising target to treat RA.

Keywords: IL-32; NF-κB; Rheumatoid arthritis; Proinflammatory cytokines

Copyright © 2015 by The American Society for BioMedicine and BM-Publisher, Inc.

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