Abstract
BackgroundAdenosine signaling is now an accepted explanation for the therapeutic mechanism of Methotrexate (MTX) in rheumatoid arthritis (RA). Adenosine receptors categorized into four subclasses: adenosine A1 receptor (ADORA1), adenosine 2a receptor (ADORA2a), adenosine 2b receptor (ADORA2B), and adenosine 3 receptor (ADORA3). Our aim is to check the mRNA expression of two adenosine receptors; ADORA2a and ADORA3 in whole blood cell of RA patients and its relation in prediction of MTX clinical response in Egyptian patients.ResultsThere was significant correlation between both ADORA2a and ADORA3 gene expression in RA patients as compared with healthy controls. The expression of ADORA2a and ADORA3 was increased in good and moderate response groups compared to no response group. There was significant correlation between both genes in mRNA expression before and after MTX treatment. Matrix metalloproteinase-3 (MMP3) concentration was significantly decreased after treatment in good and moderate response groups in comparison to non-responder group.ConclusionThe inflammatory and clinical responses in RA patients which is demonstrated by DAS28 and suppression of MMP3 were regulated by ADORA2a and ADORA3. Their level of expression can predict MTX response and their agonists may offer a novel and effective therapeutic option for RA patients.
Highlights
Adenosine signaling is an accepted explanation for the therapeutic mechanism of Methotrexate (MTX) in rheumatoid arthritis (RA)
There was significant correlation between both Adenosine 2a receptor (ADORA2a) and Adenosine 3 receptor (ADORA3) gene expression in patients group (Table 3) The expression levels of ADORA2a and ADORA3 were negatively correlated with baseline Disease Activity Score 28 (DAS28), Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and RF, and there was no correlation between gene expression with age, duration of disease, and ACPA (Table 4)
We examined the mRNA expression of ADORA2a and ADORA3 and its impact on RA disease activity in our patients to predict clinical response at 6 months of MTX
Summary
Adenosine signaling is an accepted explanation for the therapeutic mechanism of Methotrexate (MTX) in rheumatoid arthritis (RA). It is well known that high concentrations of adenosine are generated from the hydrolysis of ATP in any inflammatory or traumatic condition, adenosine behaves as a “retaliatory metabolite” that has an anti-inflammatory and immunomodulatory properties. Demonstrating this mechanism is clinically difficult because of the rapid reuptake of adenosine by cells and its conversion to inosine by adenosine deaminase present in plasma [5, 6]
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