In order to survive, H. pylori must adheres the gastric epithelial cells of its human host. For this purpose, the bacterium employs an array of adhesins, for example AlpA.
We have decoded genomes/methylomes of over 150 H. pylori strains by Single-Molecule Real-Time (SMRT) sequencing in Pacbio machines in collaboration with National Institute of Genetics, National Institute for Basic Biology, and Pacificbioscience of California.
H. pylori infection can induce angiogenesis in the pre-neoplastic cascade of events that culminates in gastric cancer, which may have important functional implications for the etiology of this disease.
Recent studies show that, in addition to Helicobacter pylori, other bacterial species such as Proteus mirabilis, Citrobacter freundii, Klebsiella pneumoniae, Enterobacter cloacae and Staphylococcus aureus are found in the gastric mucosa, either in co-infection with H. pylori or not.
Gastric cancer (GC) is the fifth most common cause of cancer death worldwide with approximately one million cases diagnosed annually.
Although Helicobacter pylori is causally associated with gastric cancer, <1% of infected individuals develop this malignancy. H. pylori infection induces gastritis that variably progresses to atrophy, intestinal metaplasia (IM), dysplasia and cancer.
