The ulcerogenic profile of Helicobacter pylori paediatric strains associated with peptic ulcer disease.

Helicobacter pylori infection is the major cause of paediatric peptic ulcer disease (PUD). In children with no other aetiology for the disease, this rare event occurs shortly after infection, presuming a still poorly understood higher susceptibility of the patient and highlighting the virulence of the implicated strain. Recently, we showed that the enhanced virulence of a group of paediatric ulcerogenic-strains result from a synergy between their ability to better adapt to the hostility of their niche and the expression of cagA, vacAs1, oipA ‘‘on’’ status, homB and jhp5621. Accordingly, these ulcerogenic strains share a particular proteome profile, providing them with better antioxidant defences, a metabolism favouring the biosynthesis of aromatic amino acids and higher motility1. Corroborating these findings, our preliminary data on electronic microscopic analyses demonstrated the presence of more abundant flagella in PUD-associated paediatric strains, in contrast to the control strain, a paediatric strain associated with non-ulcer dyspepsia (NUD). Compared with paediatric NUD-associated isolates, ulcerogenic H. pylori strains present a greater ability to induce a marked decrease in the gastric cells’ viability and to cause them severe cytoskeleton damage and mucins’ production/secretion impairment1. To uncover the underlying molecular mechanisms, we are now characterizing the modifications induced by these strains in the proteome of human gastric cells, during in vitro infection, by two-dimensional gel electrophoresis followed by mass-spectrometry.