Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10927092 | Cellular Immunology | 2005 | 10 Pages |
Abstract
Previous studies suggest that adenosine possesses anti-inflammatory properties, however, the mechanisms by which adenosine affects immune function remain unclear, particularly in the intestine. In this study, we hypothesized that adenosine directly affects pro-inflammatory gene expression in intestinal epithelial cells through modulation of NF-κB signaling. HT-29 cells were treated with adenosine prior to incubation with various stimuli and pro-inflammatory gene expression and signal transduction analyzed. Adenosine pretreatment resulted in a reduction in IL-8 expression and secretion in response to TNF-α, IL-1, LPS, and PMA. This effect was paralleled by inhibition of κB-driven luciferase expression and a reduction in recruitment of NF-κB to the IL-8 promoter. Pretreatment of HT-29 cells also resulted in reduced ERK, p38, and JNK MAPK phosphorylation, following TNF-α treatment. The observed effects in this study occurred independently of known surface adenosine receptors. This study identifies adenosine as a potent negative regulator of pro-inflammatory signaling in intestinal epithelial cells.
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Authors
Humberto B. Jijon, John Walker, Frank Hoentjen, Hugo Diaz, Julia Ewaschuk, Christian Jobin, Karen L. Madsen,