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Updated: May 17, 2026
Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
CD73 is critical for the resolution of murine colonic inflammation
Margaret S Bynoe1, Adam T Waickman, Deeqa A Mahamed
1Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA. msb76@cornell.edu
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.
Insights
CD73 deficiency exacerbates inflammatory bowel disease. Mice lacking CD73 show increased susceptibility to colitis, impaired gut barrier function, and unresolved inflammation, highlighting CD73
Area of Science:
- Immunology
- Gastroenterology
- Biochemistry
Background:
- CD73 (ecto-5'-nucleotidase) is a GPI-linked enzyme.
- It generates extracellular adenosine from AMP.
- Adenosine modulates inflammation and protects tissues.
Purpose of the Study:
- To investigate the role of CD73-derived adenosine in DSS-induced colitis.
- To determine the impact of CD73 deficiency on intestinal inflammation and barrier integrity.
Main Methods:
- Utilized CD73 knockout (CD73(-/-)) and wild-type (WT) mice.
- Induced colitis using Dextran-Sulfate-Sodium (DSS).
- Assessed weight loss, gut permeability, tight junction molecule expression, inflammatory markers (TLR9, IL-1β, TNF-α), and NF-κB activation.
Main Results:
- CD73(-/-) mice showed increased susceptibility to DSS colitis.
- Deficiency led to pronounced weight loss, delayed recovery, and increased gut permeability.
- CD73(-/-) mice exhibited decreased tight junction expression, unresolved inflammation, elevated TLR9, IL-1β, TNF-α, and constitutive NF-κB activation.
Conclusions:
- CD73 expression in the colon is crucial for controlling the severity and resolution of immune responses.
- Adenosine generated by CD73 plays a protective role in intestinal inflammation.
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