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Updated: Jun 18, 2026
A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
A model for chronic mucosal inflammation in IBD and periodontitis
Helieh S Oz1, Theresa Chen, Jeffrey L Ebersole
1MN310 Center for Oral Health Research, College of Dentistry and Department of Internal Medicine, University of Kentucky Medical Center, Lexington, KY 40536, USA. Helieh.oz@uky.edu
Background:
Chronic inflammation of mucosal surfaces is an aberrant immune response to luminal bacteria and generates an array of oxygen radicals leading to tissue destruction and loss of function, as noted in IBD and periodontitis. We hypothesized that mucosal injury after "oral delivery" of dextran sulfate sodium (DSS) or TNBS for an extended period of 18 weeks is reflected by chronic inflammatory responses in a time-dependent fashion.
Methods:
Dextran sulfate sodium was administered in the diet biweekly; TNBS or sham controls was administered orally twice a week. Additional groups received TNBS or sham injections into gingival tissue.
Results:
Animals tolerated oral applications with no severe clinical symptoms. The DSS-group developed diarrhea during the period of administration, and returned to normal during DSS abstinence. The TNBS-group developed no systemic clinical symptoms. Splenic length and weight increased in the DSS-group in a time-dependent fashion (P < 0.01) and remained normal in the TNBS-group. Colons from the DSS-group were significantly shortened (P < 0.001) and colonic weight increased compared with controls or the TNBS-group (P < 0.05). The DSS-group developed extensive dilation of the stomach wall, ileum, and megacolon, with abdominal fat deposits. In addition, the DSS-group showed dysregulated hepatic concentrations of antioxidants (i.e. cysteine, GSH, SAMe) in a time-dependent manner that correlated with a significance increase in alveolar bone resorption. Localized TNBS-mucosal delivery caused severe inflammation, granuloma formation, and rapid bone resorption.
Conclusions:
This model of mucosal stimulation eliciting chronic inflammatory responses in the gut and oral cavity mimics aspects of IBD and periodontal disease progression in patients.
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