Host-Helicobacter interactions in the mucus niche
3rd International Congress on Bacteriology and Infectious Diseases
August 04-06, 2015 Valencia, Spain

Médea Padra

Scientific Tracks Abstracts: J Bacteriol Parasitol

Abstract:

Helicobacter pylori chronically infecting half of the world’s human population and is the main etiological agent causing
gastric ulcers and cancer. Helicobacter suis colonizes the gastric mucosa and in pigs it is associated with gastritis, decreased
daily weight gain and possibly gastric ulcer disease. H. suis is also the most prevalent non-H. pylori species in the human
stomach and is associated with peptic ulcer disease, gastric mucosa-associated lymphoid tissue lymphoma and chronic gastritis.
Helicobacter bacteria are prone to developing antibiotic resistance and recurrence frequently occurs. H. pylori-infected rhesus
monkeys and human children secreting mucins with less H. pylori binding capacity develop higher H. pylori density infections
and gastritis supporting that the ability of secreted mucins to bind to H. pylori protects the gastric epithelium. Gastric mucin
turnover is impaired during H. pylori infection which in turn creates a more stable environment for H. pylori to colonize long
term. H. pylori and H. suis bound to human and pig mucins via the mucin glycans with distinctly different specificities: The
most notable difference being that H. suis bound to neutral glycans with an acidic pH optimum. This unusual binding mode
may be the reason for that H. suis in addition to colonizing the mucus layer also colonizes the acid producing parietal cells. We
found over 300 glycan structures on mucins from 16 humans and each individual carried 60-120 structures, whereas we found
around 250 structures in four pigs. Mucins differently regulated Helicobacter proliferation, gene expression and downstream
interactions with host cells. This regulation appeared to occur via at least three glycan response pathways. Both in primate
and pig models of infection, host glycosylation were altered during infection which affected the ability of these pathogens to
interact with their hosts and the outcome of the interaction. In conclusion, when a Helicobacter encounters the mucins that
build up the mucus layer; its behavior changes in a host specific manner in response to the mucin glycans. This “changed”
pathogen then interacts with the host epithelial cells which respond by changing its mucins and mucin glycans which in turn
changes the pathogen again, in constant host-pathogen adaptation and response process.

Biography :

Médea Padra is a PhD student in the Mucins in Infection and Cancer Team at the Department of Medical Biochemistry and Cell biology, University of Gothenburg,
Sweden.