Role of Helicobacter Pyroli Derived Factors in Cell Cycle Alteration of the Gastric Epithelial Cells
2662 WordsJan 31, 201811 Pages
Role of Helicobacter pyroli derived factors in cell cycle alteration of the gastric epithelial cells:
H pyroli infection relatively increases the risk of gastric adenocarcinoma and mucosa associated lymphoid tissue (MALT) lymphoma. H pyroli comprises of a heterogeneous consortium of bacterial strains which show differences in their genotype and phenotypes. Most importantly H pyroli is grouped into virulent and less virulent groups. Virulent group comprises of the type I strain which are Cag A + harbouring the cag PAI region in their genome and possess greater risk in terms of causing gastric cancer. Type II strain are Cag A – and show less virulence. H pyroli infection causes cell cycle alteration of the gastric epithelial cell by causing apoptosis and proliferation ultimately leading to increased turnover of gastric epithelial cells. A number of factors of H pyroli are responsible for this cell cycle alteration; few of them are described below.
Cag Pathogenecity Island
Cag PAI (cag pathogenecity island) is a 40kbp region of DNA in the genome of H pyroli encoding a number of virulence factor. Cag PAI has different GC content than the flanking genomic DNA indicating cag PAI to be a horizontally transferred entity. Cag PAI encodes components of T4SS that binds to B integrin and is indispensible for delivering Cag A proteins into the host epithelial cells. Almost all East Asian h pyroli strains are cag PAI + but only 60% -- 70% of the Western strains are cag PAI+. cag