Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease
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Updated: Nov 25, 2025
Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Hengameh Chloé Mirsepasi-Lauridsen1,2,3,4, Carsten Struve1, Andreas Munk Petersen5,6
1Department of Bacteria, Parasites and Fungi, Statens Serum Institut, 2300 Copenhagen, Denmark.
Background:
Phylogroup B2 Escherichia coli have been associated with ulcerative colitis (UC). In this study, we aimed to compare colonization with the UC-associated E. coli p19A in different mice strains, to investigate the role of alpha hemolysin in a UC mouse model.
Methods:
In this study, Sigirr -/- and C57BL/6 mice were chosen, and UC was induced by adding dextran sulfate sodium (DSS) to the drinking water. The mice were pre-treated with ciprofloxacin. p19A expressing luminescence and GFP, alpha-hemolysin knock out p19A-ΔhlyI II, and non-pathogenic lab E. coli DH10B were cultured in LB broth, and orally gavaged into the mice. Colonization with p19A WT was visualized using an in vivo imaging system.
Results:
p19A WT colonized the colon, ileum, Peyer's patches, liver, and spleen of infected C57BL/6 and Sigirr -/- mice. A total of 99% of the p19A WT infected C57BL/6 mice and 29% of the p19A WT infected Sigirr -/- mice survived to the 4th post infection day.
Conclusion:
UC-associated E. coli p19A WT colonized the intestines of DSS-treated mice and caused extra-intestinal infection. Hemolysin is an important factor in this pathogenesis, since isogenic hemolysin mutants did not cause the same inflammation.
Insights
Ulcerative colitis (UC)-associated Escherichia coli p19A colonizes mouse intestines and causes extra-intestinal infections. Alpha-hemolysin is crucial for this pathogenesis, as hemolysin mutants showed reduced inflammation.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Phylogroup B2 Escherichia coli strains are linked to ulcerative colitis (UC).
- The specific role of UC-associated E. coli p19A and alpha hemolysin in UC pathogenesis requires further investigation.
Purpose of the Study:
- To compare the colonization of UC-associated E. coli p19A in different mouse strains.
- To investigate the role of alpha hemolysin in a dextran sulfate sodium (DSS)-induced UC mouse model.
Main Methods:
- Sigirr-/- and C57BL/6 mice were used, with UC induced by DSS in drinking water.
- Mice were pre-treated with ciprofloxacin and orally gavaged with wild-type p19A, alpha-hemolysin knockout p19A (p19A-ΔhlyI II), or DH10B E. coli.
- Colonization was visualized using an in vivo imaging system.
Main Results:
- Wild-type p19A colonized the colon, ileum, Peyer's patches, liver, and spleen in both mouse strains.
- Survival rates were significantly higher in Sigirr-/- mice (29%) compared to C57BL/6 mice (99%) infected with p19A WT by day 4 post-infection.
Conclusions:
- UC-associated E. coli p19A colonizes DSS-treated mouse intestines and leads to extra-intestinal infections.
- Alpha hemolysin is a key virulence factor, as hemolysin mutants failed to induce similar levels of inflammation.
