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.