Alimentary TractProstaglandins prevent decreased epithelial cell proliferation associated with dextran sodium sulfate injury in mice☆,☆☆
Section snippets
Materials
Female C3H/HeJ or C3H/HeN mice were obtained from Jackson Laboratories (Bar Harbor, ME), Taconic (Germantown, NY), or Harlan Sprague–Dawley (Indianapolis, IN); housed in clear plastic cages; and fed a standard laboratory chow diet and water ad libitum. DSS (40,000-50,000 mol wt) was obtained from United States Biochemical (Cleveland, OH). Indomethacin, bromodeoxyuridine (BrdUrd), flurodeoxyuridine, and dmPGE2 were obtained from Sigma Chemical Co. (St. Louis, MO) and NS-398 from Biomol (Plymouth
Results
Administration of 3% DSS in the drinking water of female C3H mice for 5 days reproducibly resulted in injury that healed when the DSS was removed from the drinking water. The injury was characterized by blood in the stool, a loss of normal crypt architecture, thickening and edema of the muscularis (Figure 1), and patchy ulceration.
Discussion
The molecular mechanisms underlying the pathology of human IBD and DSS-induced colitis, which is a model for human IBD, remain unclear. Therefore, investigations regarding the mechanism of DSS-induced colitis are important not only for their potential applicability to human disease but in light of the common use of this model system. In our study we found two DSS-induced changes in the cecal epithelium: diminished proliferation and crypt shortening. DSS-induced crypt shortening in the cecum was
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Address requests for reprints to: Teresa G. Tessner, Ph.D., Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8124, St. Louis, Missouri 63110. Fax: (314) 362-8959.
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Supported by R01-DK33165 from the National Institutes of Health, by a grant from the Crohn's and Colitis Foundation of America (to W.F.S.), and by T32 DK07130-22 from the National Institutes of Health. (to T.G.T.).