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

Hyungjun  Hyungjun Yanga; Hengameh Chloé Lauridsen; Carsten Struve; Joannie M Allaire; Adeline Sivignon; Wayne Vogl; Else S. Bosman; Caixia Ma; Abbas Fotovati; Gregor S. Reid; Xiaoxia Li; Andreas Munk Petersen; Sébastien G. Gouin; Nicolas  Barnich; Kevan  Jacobson; Hong Bing Yu; Karen Angeliki Krogfelt; Bruce Andrew Vallance

doi:10.1080/19490976.2020.1847976

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

Hyungjun Hyungjun Yanga^*, Hengameh Chloé Lauridsen, Carsten Struve, Joannie M Allaire, Adeline Sivignon, Wayne Vogl, Else S. Bosman, Caixia Ma, Abbas Fotovati, Gregor S. Reid, Xiaoxia Li, Andreas Munk Petersen, Sébastien G. Gouin, Nicolas Barnich , Kevan Jacobson, Hong Bing Yu^*, Karen Angeliki Krogfelt^*, Bruce Andrew Vallance^*

^*Corresponding author

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

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.

Originalsprog	Engelsk
Artikelnummer	1847976
Tidsskrift	Gut Microbes
Vol/bind	12
Udgave nummer	1
ISSN	1949-0976
DOI	https://doi.org/10.1080/19490976.2020.1847976
Status	Udgivet - 10 dec. 2020
Udgivet eksternt	Ja

Link til dokument

10.1080/19490976.2020.1847976Licens: CC BY

Ulcerative Colitis associated E coli pathobionts potentiate colitis in susceptible hostsForlagets udgivne version, 5,43 MBLicens: CC BY

Citer dette

Hyungjun Yanga, H., 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), Artikel 1847976. https://doi.org/10.1080/19490976.2020.1847976

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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{\textquoteright}s disease, Inflammatory bowel disease, Ulcerative Colitis, in vivo mouse model, intestinal microbiota",

author = "{Hyungjun Yanga}, Hyungjun and 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 Andrew}",

year = "2020",

month = dec,

day = "10",

doi = "10.1080/19490976.2020.1847976",

language = "English",

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journal = "Gut Microbes",

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Hyungjun Yanga, H, 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, 1847976. https://doi.org/10.1080/19490976.2020.1847976

TY - JOUR

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

AU - Hyungjun Yanga, Hyungjun

AU - 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 Andrew

PY - 2020/12/10

Y1 - 2020/12/10

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’s disease

KW - Inflammatory bowel disease

KW - Ulcerative Colitis

KW - in vivo mouse model

KW - intestinal microbiota

U2 - 10.1080/19490976.2020.1847976

DO - 10.1080/19490976.2020.1847976

M3 - Journal article

SN - 1949-0976

VL - 12

JO - Gut Microbes

JF - Gut Microbes

IS - 1

M1 - 1847976

ER -