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J Surg Res. 2007 Jun 1;140(1):12-9. Epub 2007 Apr 6.

Loss of the tight junction protein ZO-1 in dextran sulfate sodium induced colitis.

Author information

  • 1Department of Surgery and Department of Pathology, The Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pennsylvania 17033, USA. lporitz@psu.edu

Abstract

BACKGROUND:

Inflammatory bowel disease (IBD) is associated with increased intestinal permeability and decreased expression of tight junction (TJ) proteins in the inflamed mucosa. Whether this alteration in TJ expression is a prerequisite for the development of intestinal inflammation or a secondary result of that inflammation is unknown. This study looked at the expression of the TJ protein ZO-1 and the corresponding permeability changes in dextran sulfate sodium (DSS) induced colitis in a mouse model.

MATERIALS AND METHODS:

BALB/c mice were fed 3% DSS or water for 1, 3, 5, or 7 days. The animals were weighed, stool was checked for blood, and the colon length measured. Segments of the colon were used for histology, immunohistochemistry for ZO-1, or Western blot for TJ proteins. Colonic permeability was measured using Evan's Blue dye.

RESULTS:

DSS treated animals had heme positive stools, colitis by histology, significant weight loss, and colon shortening. There was an absence of ZO-1 by Western blot in the 7-day DSS treated animals, double the amount of claudin-1 and normal cytokeratin. The loss of ZO-1 started after 1 d of DSS treatment and was followed by a significant increase in permeability to Evan's blue by day 3.

CONCLUSIONS:

The loss of ZO-1 and increased permeability preceded the development of significant intestinal inflammation suggesting that in DSS colitis alterations in the TJ complex occur before the intestinal inflammation and not as a consequence of it. These changes in the TJ complex may facilitate the development of the inflammatory infiltrate seen in colitis.

PMID:
17418867
DOI:
10.1016/j.jss.2006.07.050
[PubMed - indexed for MEDLINE]
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