Abstract
During Helicobacter pylori infection the gastric mucosa is subjected to potentially injurious factors of bacterial and host origin that alter barrier function and the regulation of epithelial cell growth. Disruption of barrier function may be due to direct bacterial actions or occur secondarily as a consequence of activation of an inflammatory response. Although H. pylori infection is normally restricted to the mucosal surface, increased gastric permeability permits further damage from bacteria and their products that gain access into the mucosa. Our research focuses on altered epithelial cell growth and death that occurs during H. pylori infection and the role that reactive oxygen species (ROS) play in these events. ROS are released by H. pylori, as well as from immune cells, and accumulate in gastric epithelial cells in response to infection, exogenous oxidative metabolites, and inflammatory cytokines. Epithelial cell apoptosis is increased in H. pylori infection and there is some evidence that antioxidants reduce ROS accumulation and programmed cell death in the epithelium during infection. During H. pylori infection both bacterial factors and the host inflammatory response serve as sources of oxidative stress, a factor that plays a role in determining the net effect on the health of the gastric epithelium. As the epithelial response is an important determinant of the outcome of infection, an understanding of the factors that disturb the epithelial barrier is relevant.
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Ding, SZ., Crowe, S.E. (2000). Helicobacter pylori and the epithelial barrier: role of oxidative injury. In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3927-4_16
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DOI: https://doi.org/10.1007/978-94-011-3927-4_16
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