CD73 Is Critical for the Resolution of Murine Colonic Inflammation
Name
Bynoe-2012-CD73 Is Critical for.pdf
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3.69 MB
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Author(s)
Bynoe, Margaret S.
Waickman, Adam T.
Mahamed, Deeqa A.
Mueller, Cynthia
Mills, Jeffrey H.
Czopik, Agnieszka
Date Issued
July 2012
Journal
Journal of Biomedicine and Biotechnology
Publisher
Hindawi Publishing Corporation
Citation
Bynoe, Margaret S. et al. “CD73 Is Critical for the Resolution of Murine Colonic Inflammation.” Journal of Biomedicine and Biotechnology 2012 (2012): 1–13. Web.
Version
Final published version
Abstract
CD73 is a glycosyl-phosphatidylinositol-(GPI-) linked membrane protein that catalyzes the extracellular dephosphorylation of adenosine monophosphate (AMP) to adenosine. Adenosine is a negative regulator of inflammation and prevents excessive cellular damage. We investigated the role of extracellular adenosine in the intestinal mucosa during the development of Dextran-Sulfate-Sodium-(DSS-)salt-induced colitis in mice that lack CD73 (CD73−/−) and are unable to synthesize extracellular adenosine. We have found that, compared to wild-type (WT) mice, CD73−/− mice are highly susceptible to DSS-induced colitis. CD73−/− mice exhibit pronounced weight loss, slower weight recovery, an increase in gut permeability, a decrease in expression of tight junctional adhesion molecules, as well as unresolved inflammation following the removal of DSS. Moreover, colonic epithelia in CD73−/− mice exhibited increased TLR9 expression, high levels of IL-1β and TNF-α, and constitutive activation of NF-κB. We conclude that CD73 expression in the colon is critical for regulating the magnitude and the resolution of colonic immune responses.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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Creative Commons Attribution
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DOI of Published Version
https://doi.org/10.1155/2012/260983
