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Std fimbriae-fucose interaction increases Salmonella-induced intestinal inflammation and prolongs colonization

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Std fimbriae-fucose interaction increases Salmonella-induced intestinal inflammation and prolongs colonization. / Suwandi, Abdulhadi; Galeev, Alibek; Riedel, René; Sharma, Samriti; Seeger, Katrin; Sterzenbach, Torsten; García Pastor, Lucía; Boyle, Erin C; Gal-Mor, Ohad; Hensel, Michael; Casadesús, Josep; Baines, John F; Grassl, Guntram A.

in: PLOS PATHOG, Jahrgang 15, Nr. 7, 07.2019, S. e1007915.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Suwandi, A, Galeev, A, Riedel, R, Sharma, S, Seeger, K, Sterzenbach, T, García Pastor, L, Boyle, EC, Gal-Mor, O, Hensel, M, Casadesús, J, Baines, JF & Grassl, GA 2019, 'Std fimbriae-fucose interaction increases Salmonella-induced intestinal inflammation and prolongs colonization', PLOS PATHOG, Jg. 15, Nr. 7, S. e1007915. https://doi.org/10.1371/journal.ppat.1007915

APA

Suwandi, A., Galeev, A., Riedel, R., Sharma, S., Seeger, K., Sterzenbach, T., García Pastor, L., Boyle, E. C., Gal-Mor, O., Hensel, M., Casadesús, J., Baines, J. F., & Grassl, G. A. (2019). Std fimbriae-fucose interaction increases Salmonella-induced intestinal inflammation and prolongs colonization. PLOS PATHOG, 15(7), e1007915. https://doi.org/10.1371/journal.ppat.1007915

Vancouver

Suwandi A, Galeev A, Riedel R, Sharma S, Seeger K, Sterzenbach T et al. Std fimbriae-fucose interaction increases Salmonella-induced intestinal inflammation and prolongs colonization. PLOS PATHOG. 2019 Jul;15(7):e1007915. https://doi.org/10.1371/journal.ppat.1007915

Bibtex

@article{ad160e3e13664fc9a581a742c408f0f0,
title = "Std fimbriae-fucose interaction increases Salmonella-induced intestinal inflammation and prolongs colonization",
abstract = "Expression of ABO and Lewis histo-blood group antigens by the gastrointestinal epithelium is governed by an α-1,2-fucosyltransferase enzyme encoded by the Fut2 gene. Alterations in mucin glycosylation have been associated with susceptibility to various bacterial and viral infections. Salmonella enterica serovar Typhimurium is a food-borne pathogen and a major cause of gastroenteritis. In order to determine the role of Fut2-dependent glycans in Salmonella-triggered intestinal inflammation, Fut2+/+ and Fut2-/- mice were orally infected with S. Typhimurium and bacterial colonization and intestinal inflammation were analyzed. Bacterial load in the intestine of Fut2-/- mice was significantly lower compared to Fut2+/+ mice. Analysis of histopathological changes revealed significantly lower levels of intestinal inflammation in Fut2-/- mice compared to Fut2+/+ mice and measurement of lipocalin-2 level in feces corroborated histopathological findings. Salmonella express fimbriae that assist in adherence of bacteria to host cells thereby facilitating their invasion. The std fimbrial operon of S. Typhimurium encodes the π-class Std fimbriae which bind terminal α(1,2)-fucose residues. An isogenic mutant of S. Typhimurium lacking Std fimbriae colonized Fut2+/+ and Fut2-/- mice to similar levels and resulted in similar intestinal inflammation. In vitro adhesion assays revealed that bacteria possessing Std fimbriae adhered significantly more to fucosylated cell lines or primary epithelial cells in comparison to cells lacking α(1,2)-fucose. Overall, these results indicate that Salmonella-triggered intestinal inflammation and colonization are dependent on Std-fucose interaction.",
keywords = "Animals, Bacterial Adhesion, Colitis/etiology, Female, Fimbriae Proteins/genetics, Fimbriae, Bacterial/genetics, Fucose/metabolism, Fucosyltransferases/deficiency, Host Microbial Interactions, Humans, Intestinal Mucosa/metabolism, Male, Mice, Mice, Inbred CBA, Mice, Knockout, Operon, Salmonella Infections, Animal/etiology, Salmonella typhimurium/genetics",
author = "Abdulhadi Suwandi and Alibek Galeev and Ren{\'e} Riedel and Samriti Sharma and Katrin Seeger and Torsten Sterzenbach and {Garc{\'i}a Pastor}, Luc{\'i}a and Boyle, {Erin C} and Ohad Gal-Mor and Michael Hensel and Josep Casades{\'u}s and Baines, {John F} and Grassl, {Guntram A}",
year = "2019",
month = jul,
doi = "10.1371/journal.ppat.1007915",
language = "English",
volume = "15",
pages = "e1007915",
journal = "PLOS PATHOG",
issn = "1553-7366",
publisher = "Public Library of Science",
number = "7",

}

RIS

TY - JOUR

T1 - Std fimbriae-fucose interaction increases Salmonella-induced intestinal inflammation and prolongs colonization

AU - Suwandi, Abdulhadi

AU - Galeev, Alibek

AU - Riedel, René

AU - Sharma, Samriti

AU - Seeger, Katrin

AU - Sterzenbach, Torsten

AU - García Pastor, Lucía

AU - Boyle, Erin C

AU - Gal-Mor, Ohad

AU - Hensel, Michael

AU - Casadesús, Josep

AU - Baines, John F

AU - Grassl, Guntram A

PY - 2019/7

Y1 - 2019/7

N2 - Expression of ABO and Lewis histo-blood group antigens by the gastrointestinal epithelium is governed by an α-1,2-fucosyltransferase enzyme encoded by the Fut2 gene. Alterations in mucin glycosylation have been associated with susceptibility to various bacterial and viral infections. Salmonella enterica serovar Typhimurium is a food-borne pathogen and a major cause of gastroenteritis. In order to determine the role of Fut2-dependent glycans in Salmonella-triggered intestinal inflammation, Fut2+/+ and Fut2-/- mice were orally infected with S. Typhimurium and bacterial colonization and intestinal inflammation were analyzed. Bacterial load in the intestine of Fut2-/- mice was significantly lower compared to Fut2+/+ mice. Analysis of histopathological changes revealed significantly lower levels of intestinal inflammation in Fut2-/- mice compared to Fut2+/+ mice and measurement of lipocalin-2 level in feces corroborated histopathological findings. Salmonella express fimbriae that assist in adherence of bacteria to host cells thereby facilitating their invasion. The std fimbrial operon of S. Typhimurium encodes the π-class Std fimbriae which bind terminal α(1,2)-fucose residues. An isogenic mutant of S. Typhimurium lacking Std fimbriae colonized Fut2+/+ and Fut2-/- mice to similar levels and resulted in similar intestinal inflammation. In vitro adhesion assays revealed that bacteria possessing Std fimbriae adhered significantly more to fucosylated cell lines or primary epithelial cells in comparison to cells lacking α(1,2)-fucose. Overall, these results indicate that Salmonella-triggered intestinal inflammation and colonization are dependent on Std-fucose interaction.

AB - Expression of ABO and Lewis histo-blood group antigens by the gastrointestinal epithelium is governed by an α-1,2-fucosyltransferase enzyme encoded by the Fut2 gene. Alterations in mucin glycosylation have been associated with susceptibility to various bacterial and viral infections. Salmonella enterica serovar Typhimurium is a food-borne pathogen and a major cause of gastroenteritis. In order to determine the role of Fut2-dependent glycans in Salmonella-triggered intestinal inflammation, Fut2+/+ and Fut2-/- mice were orally infected with S. Typhimurium and bacterial colonization and intestinal inflammation were analyzed. Bacterial load in the intestine of Fut2-/- mice was significantly lower compared to Fut2+/+ mice. Analysis of histopathological changes revealed significantly lower levels of intestinal inflammation in Fut2-/- mice compared to Fut2+/+ mice and measurement of lipocalin-2 level in feces corroborated histopathological findings. Salmonella express fimbriae that assist in adherence of bacteria to host cells thereby facilitating their invasion. The std fimbrial operon of S. Typhimurium encodes the π-class Std fimbriae which bind terminal α(1,2)-fucose residues. An isogenic mutant of S. Typhimurium lacking Std fimbriae colonized Fut2+/+ and Fut2-/- mice to similar levels and resulted in similar intestinal inflammation. In vitro adhesion assays revealed that bacteria possessing Std fimbriae adhered significantly more to fucosylated cell lines or primary epithelial cells in comparison to cells lacking α(1,2)-fucose. Overall, these results indicate that Salmonella-triggered intestinal inflammation and colonization are dependent on Std-fucose interaction.

KW - Animals

KW - Bacterial Adhesion

KW - Colitis/etiology

KW - Female

KW - Fimbriae Proteins/genetics

KW - Fimbriae, Bacterial/genetics

KW - Fucose/metabolism

KW - Fucosyltransferases/deficiency

KW - Host Microbial Interactions

KW - Humans

KW - Intestinal Mucosa/metabolism

KW - Male

KW - Mice

KW - Mice, Inbred CBA

KW - Mice, Knockout

KW - Operon

KW - Salmonella Infections, Animal/etiology

KW - Salmonella typhimurium/genetics

U2 - 10.1371/journal.ppat.1007915

DO - 10.1371/journal.ppat.1007915

M3 - SCORING: Journal article

C2 - 31329635

VL - 15

SP - e1007915

JO - PLOS PATHOG

JF - PLOS PATHOG

SN - 1553-7366

IS - 7

ER -