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Clostridium difficile  causes intestinal inflammation, which increases adenosine. We compared the expression of adenosine receptors (AR) subtypes A 1  , A  2A  , A  2B  , and A  3  in HCT-8, IEC-6 cells, and isolated intestinal epithelial cells, challenged or not with  Clostridium difficile  toxin A and B (TcdA and TcdB) or infection (CDI). In HCT-8, TcdB induced an early A 2B R expression at 6 h and a late A 2A R expression at 6 and 24 h. In addition, both TcdA and TcdB increased IL-6 expression at all time-points (peak at 6 h) and PSB603, an  A  2B R antagonist, decreased IL-6 expression and production. In isolated cecum epithelial cells, TcdA induced an early expression of  A  2B R at 2s and 6 h, followed by a late expression of A 2A R at 6 and 24 h and of A 1 R at 24 h. In CDI, A 2A  R and A  2B R expressions were increased at day 3, but not at day 7. ARs play a role in regulating inflammation during CDI by inducing an early pro-inflammatory and a late anti-inflammatory response. The timing of interventions with AR antagonist or agonists may be of relevance in treatment of CDI.

brazilian journal of medical and biological research

Clostridium difficile toxins or infection induce upregulation of adenosine receptors and IL-6 with early pro-inflammatory and late anti-inflammatory pattern