BabA-mediated adherence of pediatric ulcerogenic <i>H. pylori</i> strains to gastric mucins at neutral and acidic pH

Quintana-Hayashi, Macarena P.; Rocha, Raquel; Padra, Médea; Thorell, Anders; Jin, Chunsheng; Karlsson, Niclas G.; Roxo-Rosa, Mónica; Oleastro, Mónica; Lindén, Sara K.

doi:10.1080/21505594.2018.1532243

Cited by 16 publications

(9 citation statements)

References 47 publications

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“…We have previously demonstrated that H. suis binding occurs via two modes of adhesion: (1) to galactose-terminating structures at both neutral and acidic pH and (2) to negatively charged structures at acidic pH. 18 In contrast to the large variation in mucin-binding specificity and avidity present among H. pylori strains, 38 binding of four H. suis strains isolated from primates and pigs to pig and human mucins was very similar, 18 suggesting low inter-individual variation in binding specificity among H. suis strains. Here, we showed that the binding level of H. suis to pig gastric mucins was around sevenfold higher at pH 2 than at pH 7, regardless of the infection status of the pigs.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter suis infection alters glycosylation and decreases the pathogen growth inhibiting effect and binding avidity of gastric mucins

et al. 2019

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Helicobacter suis is the most prevalent non-Helicobacter pylori Helicobacter species in the human stomach and is associated with chronic gastritis, peptic ulcer disease, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. H. suis colonizes the gastric mucosa of 60-95% of pigs at slaughter age, and is associated with chronic gastritis, decreased weight gain, and ulcers. Here, we show that experimental H. suis infection changes the mucin composition and glycosylation, decreasing the amount of H. suisbinding glycan structures in the pig gastric mucus niche. Similarly, the H. suis-binding ability of mucins from H. pylori-infected humans is lower than that of noninfected individuals. Furthermore, the H. suis growth-inhibiting effect of mucins from both noninfected humans and pigs is replaced by a growth-enhancing effect by mucins from infected individuals/pigs. Thus, Helicobacter spp. infections impair the mucus barrier by decreasing the H. suis-binding ability of the mucins and by decreasing the antiprolific activity that mucins can have on H. suis. Inhibition of these mucus-based defenses creates a more stable and inhabitable niche for H. suis. This is likely of importance for long-term colonization and outcome of infection, and reversing these impairments may have therapeutic benefits.

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Section: Discussionmentioning

confidence: 99%

Helicobacter suis infection alters glycosylation and decreases the pathogen growth inhibiting effect and binding avidity of gastric mucins

et al. 2019

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“…hyodysenteriae growth in the presence of mucins and monosaccharides. Bacterial growth in the presence of mucins was performed as previously described (52). Mucins were dialyzed against four changes of 2 M NaCl, followed by two changes against sterile PBS.…”

Section: Methodsmentioning

confidence: 99%

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

et al. 2019

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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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“…In Western countries, infection with BabA producing strains has been associated with an increased risk for peptic ulcer disease development [91,92]. A recent study highlighted the adherence of strains with a high avidity mediated by BabA-positive pediatric ulcerogenic H. pylori strains [93].…”

Section: Virulence Factors Associated With Colonization Of Epithelmentioning

confidence: 99%

Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity

Ansari

Yamaoka

2019

Toxins

187

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Helicobacter pylori colonizes the gastric epithelial cells of at least half of the world’s population, and it is the strongest risk factor for developing gastric complications like chronic gastritis, ulcer diseases, and gastric cancer. To successfully colonize and establish a persistent infection, the bacteria must overcome harsh gastric conditions. H. pylori has a well-developed mechanism by which it can survive in a very acidic niche. Despite bacterial factors, gastric environmental factors and host genetic constituents together play a co-operative role for gastric pathogenicity. The virulence factors include bacterial colonization factors BabA, SabA, OipA, and HopQ, and the virulence factors necessary for gastric pathogenicity include the effector proteins like CagA, VacA, HtrA, and the outer membrane vesicles. Bacterial factors are considered more important. Here, we summarize the recent information to better understand several bacterial virulence factors and their role in the pathogenic mechanism.

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BabA-mediated adherence of pediatric ulcerogenic H. pylori strains to gastric mucins at neutral and acidic pH

Cited by 16 publications

References 47 publications

Helicobacter suis infection alters glycosylation and decreases the pathogen growth inhibiting effect and binding avidity of gastric mucins

Helicobacter suis infection alters glycosylation and decreases the pathogen growth inhibiting effect and binding avidity of gastric mucins

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

Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity

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