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Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts

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Harvard

Yang, H, Mirsepasi-Lauridsen, HC, Struve, C, Allaire, JM, Sivignon, A, Vogl, W, Bosman, ES, Ma, C, Fotovati, A, Reid, GS, Li, X, Petersen, AM, Gouin, SG, Barnich, N, Jacobson, K, Yu, HB, Krogfelt, KA & Vallance, BA 2020, 'Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts', Gut Microbes, bind 12, nr. 1, s. 1847976. https://doi.org/10.1080/19490976.2020.1847976

APA

Yang, H., Mirsepasi-Lauridsen, H. C., Struve, C., Allaire, J. M., Sivignon, A., Vogl, W., Bosman, E. S., Ma, C., Fotovati, A., Reid, G. S., Li, X., Petersen, A. M., Gouin, S. G., Barnich, N., Jacobson, K., Yu, H. B., Krogfelt, K. A., & Vallance, B. A. (2020). Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts. Gut Microbes, 12(1), 1847976. https://doi.org/10.1080/19490976.2020.1847976

CBE

Yang H, Mirsepasi-Lauridsen HC, Struve C, Allaire JM, Sivignon A, Vogl W, Bosman ES, Ma C, Fotovati A, Reid GS, Li X, Petersen AM, Gouin SG, Barnich N, Jacobson K, Yu HB, Krogfelt KA, Vallance BA. 2020. Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts. Gut Microbes. 12(1):1847976. https://doi.org/10.1080/19490976.2020.1847976

MLA

Vancouver

Yang H, Mirsepasi-Lauridsen HC, Struve C, Allaire JM, Sivignon A, Vogl W o.a. Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts. Gut Microbes. 2020 dec 1;12(1):1847976. https://doi.org/10.1080/19490976.2020.1847976

Author

Yang, Hyungjun ; Mirsepasi-Lauridsen, Hengameh Chloé ; Struve, Carsten ; Allaire, Joannie M ; Sivignon, Adeline ; Vogl, Wayne ; Bosman, Else S ; Ma, Caixia ; Fotovati, Abbas ; Reid, Gregor S ; Li, Xiaoxia ; Petersen, Andreas Munk ; Gouin, Sébastien G ; Barnich, Nicolas ; Jacobson, Kevan ; Yu, Hong Bing ; Krogfelt, Karen Angeliki ; Vallance, Bruce A. / Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts. I: Gut Microbes. 2020 ; Bind 12, Nr. 1. s. 1847976.

Bibtex

@article{fa27e061b5dc4a36afd20574048bdf3a,
title = "Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts",
abstract = "Ulcerative colitis (UC) is a chronic inflammatory condition linked to intestinal microbial dysbiosis, including the expansion of E. coli strains related to extra-intestinal pathogenic E. coli. These {"}pathobionts{"} exhibit pathogenic properties, but their potential to promote UC is unclear due to the lack of relevant animal models. Here, we established a mouse model using a representative UC pathobiont strain (p19A), and mice lacking single immunoglobulin and toll-interleukin 1 receptor domain (SIGIRR), a deficiency increasing susceptibility to gut infections. Strain p19A was found to adhere to the cecal mucosa of Sigirr -/- mice, causing modest inflammation. Moreover, it dramatically worsened dextran sodium sulfate-induced colitis. This potentiation was attenuated using a p19A strain lacking α-hemolysin genes, or when we targeted pathobiont adherence using a p19A strain lacking the adhesin FimH, or following treatment with FimH antagonists. Thus, UC pathobionts adhere to the intestinal mucosa, and worsen the course of colitis in susceptible hosts.",
keywords = "Crohn&#8217, Inflammatory bowel disease, Ulcerative Colitis, in vivo mouse model, intestinal microbiota, s disease",
author = "Hyungjun Yang and Mirsepasi-Lauridsen, {Hengameh Chlo{\'e}} and Carsten Struve and Allaire, {Joannie M} and Adeline Sivignon and Wayne Vogl and Bosman, {Else S} and Caixia Ma and Abbas Fotovati and Reid, {Gregor S} and Xiaoxia Li and Petersen, {Andreas Munk} and Gouin, {S{\'e}bastien G} and Nicolas Barnich and Kevan Jacobson and Yu, {Hong Bing} and Krogfelt, {Karen Angeliki} and Vallance, {Bruce A}",
year = "2020",
month = dec,
day = "1",
doi = "10.1080/19490976.2020.1847976",
language = "English",
volume = "12",
pages = "1847976",
journal = "Gut Microbes",
issn = "1949-0976",
publisher = "Landes Bioscience",
number = "1",

}

RIS

TY - JOUR

T1 - Ulcerative Colitis-associated E. coli pathobionts potentiate colitis in susceptible hosts

AU - Yang, Hyungjun

AU - Mirsepasi-Lauridsen, Hengameh Chloé

AU - Struve, Carsten

AU - Allaire, Joannie M

AU - Sivignon, Adeline

AU - Vogl, Wayne

AU - Bosman, Else S

AU - Ma, Caixia

AU - Fotovati, Abbas

AU - Reid, Gregor S

AU - Li, Xiaoxia

AU - Petersen, Andreas Munk

AU - Gouin, Sébastien G

AU - Barnich, Nicolas

AU - Jacobson, Kevan

AU - Yu, Hong Bing

AU - Krogfelt, Karen Angeliki

AU - Vallance, Bruce A

PY - 2020/12/1

Y1 - 2020/12/1

N2 - Ulcerative colitis (UC) is a chronic inflammatory condition linked to intestinal microbial dysbiosis, including the expansion of E. coli strains related to extra-intestinal pathogenic E. coli. These "pathobionts" exhibit pathogenic properties, but their potential to promote UC is unclear due to the lack of relevant animal models. Here, we established a mouse model using a representative UC pathobiont strain (p19A), and mice lacking single immunoglobulin and toll-interleukin 1 receptor domain (SIGIRR), a deficiency increasing susceptibility to gut infections. Strain p19A was found to adhere to the cecal mucosa of Sigirr -/- mice, causing modest inflammation. Moreover, it dramatically worsened dextran sodium sulfate-induced colitis. This potentiation was attenuated using a p19A strain lacking α-hemolysin genes, or when we targeted pathobiont adherence using a p19A strain lacking the adhesin FimH, or following treatment with FimH antagonists. Thus, UC pathobionts adhere to the intestinal mucosa, and worsen the course of colitis in susceptible hosts.

AB - Ulcerative colitis (UC) is a chronic inflammatory condition linked to intestinal microbial dysbiosis, including the expansion of E. coli strains related to extra-intestinal pathogenic E. coli. These "pathobionts" exhibit pathogenic properties, but their potential to promote UC is unclear due to the lack of relevant animal models. Here, we established a mouse model using a representative UC pathobiont strain (p19A), and mice lacking single immunoglobulin and toll-interleukin 1 receptor domain (SIGIRR), a deficiency increasing susceptibility to gut infections. Strain p19A was found to adhere to the cecal mucosa of Sigirr -/- mice, causing modest inflammation. Moreover, it dramatically worsened dextran sodium sulfate-induced colitis. This potentiation was attenuated using a p19A strain lacking α-hemolysin genes, or when we targeted pathobiont adherence using a p19A strain lacking the adhesin FimH, or following treatment with FimH antagonists. Thus, UC pathobionts adhere to the intestinal mucosa, and worsen the course of colitis in susceptible hosts.

KW - Crohn&#8217

KW - Inflammatory bowel disease

KW - Ulcerative Colitis

KW - in vivo mouse model

KW - intestinal microbiota

KW - s disease

U2 - 10.1080/19490976.2020.1847976

DO - 10.1080/19490976.2020.1847976

M3 - Journal article

C2 - 33258388

VL - 12

SP - 1847976

JO - Gut Microbes

JF - Gut Microbes

SN - 1949-0976

IS - 1

ER -

ID: 61405328