Description
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.
; Saraiva-Pava, Kathy 
