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, Vol. 15, No. 7, 07.2019, p. e1007915.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -