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

Artikel i vetenskaplig tidskrift
Författare Médea Padra
Barbara Adamczyk
Bram Flahou
Mattias Erhardsson
Gurdeep Chahal
Annemieke Smet
Chunsheng Jin
Anders Thorell
Richard Ducatelle
Freddy Haesebrouck
Niclas G. Karlsson
Sara K. Lindén
Publicerad i Mucosal Immunology
Volym 12
Sidor 784-794
ISSN 1933-0219
Publiceringsår 2019
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 784-794
Språk en
Länkar https://doi.org/10.1038/s41385-019-...
Ämneskategorier Biologiska vetenskaper, Medicinska grundvetenskaper

Sammanfattning

© 2019, The Author(s). 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. suis-binding 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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