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Updated: Jan 18, 2026

Trichuris muris Infection: A Model of Type 2 Immunity and Inflammation in the Gut
Published on: May 24, 2011
Chlamydia muridarum Infection Impacts Murine Models of Intestinal Inflammation and Cancer
Chlamydia muridarum (Cm) infection impacts mouse models of intestinal inflammation and tumorigenesis differently. Cm attenuated Citrobacter rodentium colitis but worsened Il10-/- mouse colitis, and reduced ApcMin/+ mouse colon tumors.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Chlamydia muridarum (Cm) is a prevalent pathogen in mouse research colonies.
- Its impact on experimental models of gastrointestinal disease is not well understood.
- Persistent colonization of the murine gut by Cm necessitates investigation into its effects.
Purpose of the Study:
- To evaluate the impact of Cm colonization on established mouse models of intestinal inflammation and tumorigenesis.
- To assess Cm's influence on Citrobacter rodentium (Cr), Trichuris muris (Tm), and Il10-/- mouse models.
- To determine Cm's effect on ApcMin/+ mice undergoing DSS-induced tumorigenesis.
Main Methods:
- Mice (C57BL/6J, Il10-/- , ApcMin/+) were colonized with Cm via cohousing.
- Colonized mice were challenged with Cr, Tm, or DSS.
- Il10-/- mice were also assessed with and without Helicobacter hepaticus co-infection.
- Lesion severity and tumor development were evaluated using a semi-quantitative scoring system.
Main Results:
- Cm infection attenuated Cr-associated colitis (p=0.03).
- Cm had no significant effect on Tm-associated pathology (p=0.22).
- Cm worsened colitis in Il10-/- mice lacking H. hepaticus (p=0.007).
- Cm reduced DSS-induced colonic tumorigenesis in ApcMin/+ mice (p=0.004).
Conclusions:
- Cm colonization differentially affects various models of intestinal inflammation and tumorigenesis.
- The presence of Cm in mouse colonies should be considered a potential variable in experimental outcomes.
- Further research is needed to elucidate the mechanisms behind Cm's varied effects.
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