Session Type: Abstract Submissions (ACR)
Background/Purpose: Chemerin is a specific chemoattractant for macrophages and dendritic cells (DC). In addition, it can rapidly stimulate macrophage adhesion to extracellular matrix proteins and adhesion molecules and is able to activate fibroblast-like synoviocytes (FLS), suggesting a role in the pathogenesis of rheumatoid arthritis (RA). Chemerin is also an adipocytokine that has been related to the inflammatory state of endothelial cells and as such could be involved in the changes in endothelial cells in RA and perhaps increased cardiovascular morbidity. We investigated whether anti-TNF treatment affects chimeric levels.
Methods: 49 patients with active RA (disease activity score evaluated in 28 joints (DAS28)) ≥3.2) were started on adalimumab therapy. Blood was drawn from patients while fasting at baseline and 16 weeks after treatment. Chemerin serum levels were measured by ELISA and related to disease activity, mediators of inflammation and known risk factors for cardiovascular disease
Results: Adalimumab therapy significantly reduced chemerin serum levels, which was correlated with the reduction in DAS28 (r=0.37, p=0.009), ESR (r=0.55 p<0.001), CRP (r=0.40, p=0.005). In addition, the decrease in chemerin serum levels after anti-TNF treatment was associated with the decrease in serum levels of IL-6 (r=0.39, p=0.033) and macrophage migration inhibitory factor (MIF) (r=0.31, p=0.049). Baseline chemerin serum levels were not related to traditional risk factors for atherosclerosis, except perhaps for smoking (p=0.07).
The present study suggests that anti-TNF therapy may exert its beneficial effects on synovial inflammation and cardiovascular morbidity in part via an effect on chemerin levels.
M. M. Herenius,
A. S. F. Oliveira,
C. A. Wijbrandts,
P. P. Tak,
Employee of GlaxoSmithKline,
M. C. Lebre,
« Back to 2012 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/anti-tumor-necrosis-factor-therapy-reduces-serum-levels-of-chemerin-in-rheumatoid-arthritis-a-new-mechanism-by-which-anti-tumor-necrosis-factor-might-reduce-inflammation/