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Published on: April 21, 2015
Variable impact of CD39 in experimental murine colitis.
Beat M Künzli1, Pascal O Berberat, Karen Dwyer
1Transplant Institute and Gastroenterology Division, Beth Israel Deaconess Medical Centre/Harvard Medical School, Harvard University, Boston, MA 02215, USA.
Digestive Diseases and Sciences
|October 12, 2010
Summary
Global deletion of CD39 ectonucleotidase attenuated trinitrobenzene sulfonic acid-induced colitis in mice, improving survival and reducing inflammation. However, oxazolone-induced colitis outcomes remained comparable between CD39-null and wild-type mice.
Area of Science:
- Immunology
- Gastroenterology
- Molecular Biology
Background:
- Immune dysregulation drives inflammatory bowel diseases (IBD), causing intestinal inflammation and vascular injury.
- CD39, an ectonucleotidase on T regulatory cells and dendritic cells, modulates immune responses relevant to IBD.
- CD39 genetic variations are linked to Crohn's disease, and its absence exacerbates experimental colitis.
Purpose of the Study:
- To investigate the impact of global CD39 deletion on various experimental colitis models.
- To understand CD39's role in modulating immune responses within the intestinal environment.
Main Methods:
- Experimental colitis induced via intrarectal administration of trinitrobenzene sulfonic acid (TNBS) or oxazolone in CD39-null and wild-type mice.
- Analysis of clinical scores, morphology, molecular parameters, and immune cell populations (FACS) in lamina propria mononuclear cells (LPMC).
- Examination of CD39 expression in human IBD biopsies.
Main Results:
- CD39-null mice exhibited improved survival and reduced MPO activity in TNBS-induced colitis compared to wild-type.
- TNBS colitis in CD39-null mice showed increased T-cells and TNF-α mRNA in LPMC, despite overall improvement.
- Oxazolone-induced colitis outcomes were similar in both CD39-null and wild-type mice.
- High CD39 expression was observed in human ulcerative colitis and Crohn's disease tissues.
Conclusions:
- CD39 deficiency attenuates TNBS-induced colitis, suggesting a protective role in this model.
- Oxazolone-induced colitis is not significantly affected by CD39 deletion.
- Impaired adaptive immunity in CD39-null mice may protect against hapten-mediated Th1-type colitis.
- CD39 is highly expressed in clinical IBD, warranting further investigation.
