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Role of Sialic Acid in Brachyspira hyodysenteriae Adhesion to Pig Colonic Mucins

Journal article
Authors Macarena P Quintana-Hayashi
Vignes Venkatakrishnan
F. Haesebrouck
Sara K. Lindén
Published in Infection and Immunity
Volume 87
Issue 7
ISSN 0019-9567
Publication year 2019
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Language en
Keywords Brachyspira hyodysenteriae, adhesion, colon, mucins, pig, sialic acid, helicobacter-pylori, swine-dysentery, antimicrobial susceptibility, treponema-hyodysenteriae, gnotobiotic pigs, vibrio-cholerae, mucosal, barrier, gastric mucins, muc1 mucin, glycosylation, Immunology, Infectious Diseases
Subject categories Immunology in the medical area


Infection with Brachyspira hyodysenteriae results in mucoid hemorrhagic diarrhea. This pathogen is associated with the colonic mucus layer, mainly composed of mucins. Infection regulates mucin O-glycosylation in the colon and increases mucin secretion as well as B. hyodysenteriae binding sites on mucins. Here, we analyzed potential mucin epitopes for B. hyodysenteriae adhesion in the colon, as well as the effect of colonic mucins on bacterial growth. Associations between B. hyodysenteriae binding to pig colonic mucins and mucin glycan data showed that B. hyodysenteriae binding was associated with the presence of N-glycolylneuraminic acid (NeuGc) on mucins. The role of sialic acid in B. hyodysenteriae adhesion was analyzed after the removal of sialic acid residues on the mucins by enzymatic treatment with sialidase A, which decreased bacterial binding to the mucins. The effect of pig colonic mucins on B. hyodysenteriae growth was determined in carbohydrate-free medium. B. hyodysenteriae growth increased in the presence of mucins from two out of five infected pigs, suggesting utilization of mucins as a carbon source for growth. Additionally, bacterial growth was enhanced by free sialic acid and N-acetylglucosamine. The results highlight a role of sialic acid as an adhesion epitope for B. hyodysenteriae interaction with colonic mucins. Furthermore, the mucin response and glycosylation changes exerted in the colon during B. hyodysenteriae infection result in a potentially favorable environment for pathogen growth in the intestinal mucus layer.

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