PLoS pathogens, 2019-07-01, Vol.15 (7), p.e1007915-e1007915
Expression of ABO and Lewis histo-blood group antigens by the gastrointestinal epithelium is governed by an alpha-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 pi-class Std fimbriae which bind terminal alpha(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 alpha(1,2)-fucose. Overall, these results indicate that Salmonella-triggered intestinal inflammation and colonization are dependent on Std-fucose interaction.
ABO system ; Analysis ; Animals ; Antigens ; Bacteria ; Bacterial Adhesion ; Biology and Life Sciences ; Blood groups ; Care and treatment ; Cell lines ; Colitis - etiology ; Colitis - metabolism ; Colitis - microbiology ; Colonization ; Epidemiology ; Epithelial cells ; Epithelium ; Evolutionary biology ; Female ; Fimbriae Proteins - genetics ; Fimbriae Proteins - metabolism ; Fimbriae, Bacterial - genetics ; Fimbriae, Bacterial - metabolism ; Fucose ; Fucose - metabolism ; Fucosyltransferases - deficiency ; Fucosyltransferases - genetics ; Fucosyltransferases - metabolism ; Funding ; FUT2 gene ; Gastroenteritis ; Gene expression ; Genomics ; Glycosylation ; Hospitals ; Host Microbial Interactions ; Host-bacteria relationships ; Humans ; Infections ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - microbiology ; Intestinal Mucosa - pathology ; Intestine ; Laboratory animals ; Levels ; Life Sciences & Biomedicine ; Lipocalin ; Male ; Medical schools ; Medicine and Health Sciences ; Mice ; Mice, Inbred CBA ; Mice, Knockout ; Microbiology ; Microbiota ; Mucin ; Operon ; Parasitology ; Pathogens ; Pili ; Polysaccharides ; Proteins ; Research ; Risk factors ; Salmonella ; Salmonella Infections, Animal - etiology ; Salmonella Infections, Animal - metabolism ; Salmonella Infections, Animal - microbiology ; Salmonella typhimurium - genetics ; Salmonella typhimurium - pathogenicity ; Salmonella typhimurium - physiology ; Science & Technology ; Virology
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