Journal
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH
Volume 53, Issue 9, Pages -Publisher
ASSOC BRAS DIVULG CIENTIFICA
DOI: 10.1590/1414-431X20209877
Keywords
Clostridium difficile; Clostridium difficile toxins; Adenosine; A(2A) adenosine receptor; A(2B) adenosine receptor
Categories
Funding
- Brazilian National Council for Scientific and Technological Development, PRONEX/FUNCAP/CNPq [PR2 0101-00060. 01.00/15]
- [R21A119418]
- [U19AI109776]
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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 2 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.
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