@article {MUSACCHIO1575, author = {ESTELLA MUSACCHIO and CHIARA VALVASON and CONSTANTIN BOTSIOS and FRANCESCA OSTUNI and ANTONIO FURLAN and ROBERTA RAMONDA and VALENTINA MODESTI and LEONARDO SARTORI and LEONARDO PUNZI}, title = {The Tumor Necrosis Factor-α-blocking Agent Infliximab Inhibits Interleukin 1{\ss} (IL-1{\ss}) and IL-6 Gene Expression in Human Osteoblastic Cells}, volume = {36}, number = {8}, pages = {1575--1579}, year = {2009}, doi = {10.3899/jrheum.081321}, publisher = {The Journal of Rheumatology}, abstract = {Objective. Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine involved in the pathogenesis of several rheumatic diseases, including rheumatoid arthritis (RA), associated with systemic bone loss and subchondral bone erosions. TNF-α-blocking agents such as infliximab have been successful in treatment of disease-modifying antirheumatic drug-resistant rheumatic diseases. Infliximab therapy in RA also had beneficial effects on local bone destruction and bone mineral density. We assessed effects of infliximab treatment on the bone tissue compartment and cytokine profile expression in vitro. Methods. Osteoblast-like cells were exposed for 24 h to sera of RA patients collected at baseline and after 1 month (T1) and 3 years (T2) of infliximab treatment. Total RNA was extracted, and expression of interleukin 1{\ss} (IL-1{\ss}), IL-6, and osteoprotegerin (OPG) was measured by RT-PCR. Results. IL-1{\ss} gene expression was significantly reduced by the T1 serum, and the same decrease was elicited by the T2 serum. IL-6 downregulation was evident with the T2 serum. OPG was unaffected. Conclusion. The finding of downregulation of inflammatory cytokines was interesting, particularly IL-6, which plays a crucial role in arthritis-related bone loss due to its involvement in osteoclast recruitment and activation. These results may represent a biological explanation and a link for the clinical observation of the beneficial effects of anti-TNF-α agents on the progression of rheumatic diseases at the bone level.}, issn = {0315-162X}, URL = {https://www.jrheum.org/content/36/8/1575}, eprint = {https://www.jrheum.org/content/36/8/1575.full.pdf}, journal = {The Journal of Rheumatology} }