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To investigate the expression of adenosine A3 receptor (A3AR) in human colonic epithelial cells and the effects of A3AR activation on tumor necrosis factor alpha (TNF-  α  -) induced inflammation in order to determine its mechanism of action in human colonic epithelial cells, human colonic epithelial cells (HT-29 cells) were treated with different concentrations of 2-Cl-IB-MECA prior to TNF-  α   stimulation, followed by analysis of NF-  κ  B signaling pathway activation and downstream IL-8 and IL-1  β   production. A3AR mRNA and protein were expressed in HT-29 cells and not altered by changes in TNF-  α   or 2-Cl-IB-MECA. Pretreatment with 2-Cl-IB-MECA prior to stimulation with TNF-  α   attenuated NF-  κ  B p65 nuclear translocation as p65 protein decreased in the nucleus of cells and increased in the cytoplasm, inhibited the degradation of I  κ  B-  α  , and reduced phosphorylated-I  κ  B-  α   level significantly, compared to TNF-  α  -only-treated groups. Furthermore, 2-Cl-IB-MECA significantly decreased TNF-  α  -stimulated IL-8 and IL-1  β   mRNA expression and secretion, compared to the TNF-  α  -only treated group. These results confirm that A3AR is expressed in human colonic epithelial cells and demonstrate that its activation has an anti-inflammatory effect, through the inhibition of NF-  κ  B signaling pathway, which leads to inhibition of downstream IL-8 and IL-1  β   expression. Therefore, A3AR activation may be a potential treatment for gut inflammatory diseases such as inflammatory bowel disease.

mediators of inflammation

Activation of Adenosine A3 Receptor Alleviates TNF-α-Induced Inflammation through Inhibition of the NF-κB Signaling Pathway in Human Colonic Epithelial Cells