Hengameh Chloé Mirsepasi-Lauridsen1,2,3,4, Carsten Struve1, Andreas Munk Petersen5,6, Karen Angeliki Krogfelt4,7. 1. Department of Bacteria, Parasites and Fungi, Statens Serum Institut, 2300 Copenhagen, Denmark. 2. Department of Biology, University of Copenhagen, 2200 Copenhagen, Denmark. 3. Division of Gastroenterology, BC Children's Hospital, University of British Columbia, Vancouver, BC V6H 3N1, Canada. 4. Institute of Molecular and Medical Biology, Roskilde University, 4000 Roskilde, Denmark. 5. Department of Gastroenterology, Copenhagen University Hospital Hvidovre, 2650 Hvidovre, Denmark. 6. Department of Clinical Microbiology, Copenhagen University Hospital Hvidovre, 2650 Hvidovre, Denmark. 7. Department of Virus & Microbiological Special Diagnostics, Statens Serum Institute, 2300 Copenhagen, Denmark.
Abstract
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.
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. colip19A 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 p19AWT infected C57BL/6 mice and 29% of the p19AWT infectedSigirr -/- mice survived to the 4th post infection day. CONCLUSION: UC-associated E. colip19A 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.
Authors: Chin Wen Png; Sara K Lindén; Kristen S Gilshenan; Erwin G Zoetendal; Chris S McSweeney; Lindsay I Sly; Michael A McGuckin; Timothy H J Florin Journal: Am J Gastroenterol Date: 2010-07-20 Impact factor: 10.864
Authors: Hui Xiao; Muhammet Fatih Gulen; Jinzhong Qin; Jianhong Yao; Katarzyna Bulek; Danielle Kish; Cengiz Zubeyir Altuntas; David Wald; Caixia Ma; Hang Zhou; Vincent K Tuohy; Robert L Fairchild; Carol de la Motte; Daniel Cua; Bruce A Vallance; Xiaoxia Li Journal: Immunity Date: 2007-03-29 Impact factor: 31.745