Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease

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Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease. / Mirsepasi-Lauridsen, Hengameh Chloé; Struve, Carsten; Petersen, Andreas Munk; Krogfelt, Karen Angeliki.

In: Microorganisms, Vol. 8, No. 12, 1971, 2020.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Mirsepasi-Lauridsen, HC, Struve, C, Petersen, AM & Krogfelt, KA 2020, 'Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease', Microorganisms, vol. 8, no. 12, 1971. https://doi.org/10.3390/microorganisms8121971

APA

Mirsepasi-Lauridsen, H. C., Struve, C., Petersen, A. M., & Krogfelt, K. A. (2020). Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease. Microorganisms, 8(12), [1971]. https://doi.org/10.3390/microorganisms8121971

Vancouver

Mirsepasi-Lauridsen HC, Struve C, Petersen AM, Krogfelt KA. Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease. Microorganisms. 2020;8(12). 1971. https://doi.org/10.3390/microorganisms8121971

Author

Mirsepasi-Lauridsen, Hengameh Chloé ; Struve, Carsten ; Petersen, Andreas Munk ; Krogfelt, Karen Angeliki. / Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease. In: Microorganisms. 2020 ; Vol. 8, No. 12.

Bibtex

@article{3d4ab5b476ba4d02ae5efc9ce903d6be,
title = "Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease",
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.",
author = "Mirsepasi-Lauridsen, {Hengameh Chlo{\'e}} and Carsten Struve and Petersen, {Andreas Munk} and Krogfelt, {Karen Angeliki}",
year = "2020",
doi = "10.3390/microorganisms8121971",
language = "English",
volume = "8",
journal = "Microorganisms",
issn = "2076-2607",
publisher = "M D P I AG",
number = "12",

}

RIS

TY - JOUR

T1 - Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease

AU - Mirsepasi-Lauridsen, Hengameh Chloé

AU - Struve, Carsten

AU - Petersen, Andreas Munk

AU - Krogfelt, Karen Angeliki

PY - 2020

Y1 - 2020

N2 - 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.

AB - 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.

U2 - 10.3390/microorganisms8121971

DO - 10.3390/microorganisms8121971

M3 - Journal article

C2 - 33322398

VL - 8

JO - Microorganisms

JF - Microorganisms

SN - 2076-2607

IS - 12

M1 - 1971

ER -

ID: 261150462