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| Although most infections are asymptomatic, about 10% of cases of H. pylori colonization lead to illness. H. pylori is a major cause of chronic active gastritis and peptic ulcer disease and is also an early risk factor for gastric cancer. Infections are occasionally cleared spontaneously after a brief acute phase, but many last for years or decades, and it is these long-term infections that are most often implicated in disease (Kusters et al., 2006). The persistence of the H. pylori infection is surprising considering that the bacterium stimulates marked humoral and cellular immune responses in the human host, which are insufficient to clear the infection (Harry L. T. Mobley and Hazell , 2001; Suerbaum and Michetti , 2002).
1.1.4 Ecological niche The means by which H. pylori occupies its gastric niche and the basis for its biochemical capabilities and requirements is of great fundamental interest. A thorough understanding of H. pylori physiology and metabolism could lead to new and better drug therapies, to the identification of potential targets for therapeutic intervention, or to an effective vaccine. Understanding how the organism colonizes and persists in the host is an important step in fully understanding its pathogenesis. H. pylori have adapted to survive in the very specific and unique ecological niche of the human stomach (Lee and Josenhans, 2005; Sachs et al., 2003; Go, 2002). Because of the presence of gastric acid which rapidly destroys the majority of bacteria, the stomach is typically colonized only by transient oral flora. H. pylori appears to have evolved specific mechanisms to assist its survival in this hostile environment. These factors include the ability to swim well in the thick, protective mucus gel layer, the ability to transiently survive exposure to acid, and the ability to attach to the epithelial cell layer to prevent the bacteria from being washed out of the stomach through the mechanical action of peristalsis. As a result, other infectious agents do not appear to successfully compete with H. pylori in this environment (Sachs et al., 2003). Major non-specific host defenses against microbial colonization of the stomach are gastric acid, peristalsis, and the continual shedding of the cells and mucus lining of the gastric surface. Go, M. F., Review article: Natural history and epidemiology of Helicobacter pylori infection, Aliment Pharmacol Ther, 16 Suppl 1, 3-15, 2002. Harry L. T. Mobley, G. L. M. and S. L. Hazell, Helicobacter pylori Physiology and Genetics, ASM Press, 2001, Kusters, J. G., A. H. van Vliet, and E. J. Kuipers, Pathogenesis of Helicobacter pylori infection, Clin Microbiol Rev, 19, 449-490, 2006, Lee, S. K,, and C. Josenhans, Helicobacter pylori and the innate immune system, Int J Med Microbiol, 295, 325-334, 2005, Sachs, G., D. L. Weeks, K. Melchers, and D. R. Scott, The gastric biology of Helicobacter pylori, Annu Rev Physiol, 65, 349-369, 2003, Suerbaum, S., and P. Michetti, Helicobacter pylori infection, N Engl J Med, 347, 1175-1186, 2002. |
Although most infections are asymptomatic, about 10% of cases of H. pylori colonization lead to illness (34). H. pylori is a major cause of chronic active gastritis and peptic ulcer disease (80, 81, 141, 150) and is also an early risk factor for gastric cancer (127, 128). Infections are occasionally cleared spontaneously after a brief acute phase, but many last for years or decades, and it is these long-term infections that are most often implicated in disease (16, 159). The persistence of the H. pylori infection is surprising considering that the bacterium stimulates marked humoral and cellular immune responses in the human host, which are insufficient to clear the infection (26).
[page 6] Ecological niche The means by which H. pylori occupies its gastric niche and the basis for its biochemical capabilities and requirements is of great fundamental interest. A thorough understanding of H. pylori physiology and metabolism could lead to new and better drug therapies, to the identification of potential targets for therapeutic intervention, or to an effective vaccine. Understanding how the organism colonizes and persists in the host is an important step in fully understanding its pathogenesis. H. pylori has adapted to survive in the very specific and unique ecological niche of the human stomach. Because of the presence of gastric acid, which rapidly destroys the majority of bacteria, the stomach is typically colonized only by transient oral flora (156). H. pylori appears to have evolved specific mechanisms to assist its survival in the hostile environment. These factors include the ability to swim well in the thick, protective mucus gel layer, the ability to transiently survive exposure to acid, and the ability to attach to the epithelial cell layer to prevent the bacteria from being washed out of the stomach through the mechanical action of peristalsis. As a result, other infectious agents do not appear to successfully compete with H. pylori in this environment. Major non-specific host defenses against microbial colonization of the stomach are gastric acid, peristalsis, and the continual shedding of the cells and mucus lining the gastric surface (34). 16. Blaser, M. J. 1992. Perspectives on the pathogenesis of Helicobacter pylori infections, p. 276-280. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and Gastroduodenal Disease, 2nd ed. Blackwell Scientific Publishing, Oxford. 26. Chen, M., and A. Lee. 1993. Vaccination possibilities and probabilities, p. 158-169. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston. 34. Cover, T. L., D. E. Berg, M. J. Blaser, and H. L. T. Mobley. 2001. H. pylori pathogenesis, p. 509-558. In E. A. Groisman (ed.), Principles of Bacterial Pathogenesis. Academic Press, San Diego. 80. Jones, D. M., A. Curry, and A. J. Fox. 1985. An ultrastructural study of the gastric Campylobacter-like organism 'Campylobacter pyloridis'. Journal of General Microbiology 131:2335-41. 81. Jones, D. M., A. M. Lessells, and J. Eldridge. 1984. Campylobacter like organisms on the gastric mucosa: culture, histological, and serological studies. Journal of Clinical Pathology 37:1002-6. 127. Nomura, A., G. N. Stemmermann, P.-H. Chyou, I. Kato, G. I. Perez- Perez, and M. J. Blaser. 1991. Helicobacter pylori infection and gastric carcinoma among Japanese Americans in Hawaii. The New England Journal of Medicine 325:1132-6. 128. Parsonnet, J., G. D. Friedman, D. P. Vandersteen, Y. Chang, J. H. Vogelman, N. Orentreich, and R. K. Sibley. 1991. Helicobacter pylori infection and the risk of gastric carcinoma. The New England Journal of Medicine 325:1127-31. 141. Rollason, T. P., J. Stone, and J. M. Rhodes. 1984. Spiral organisms in endoscopic biopsies of the human stomach. Journal of Clinical Pathology 37:23- 6. 150. Stark, R. M., J. Greenman, and M. R. Millar. 1995. Physiology and biochemistry of Helicobacter pylori. British Journal of Biomedical Science 52:282-290. 156. Thompkins, D. S. 1992. Isolation and characterization of Helicobacter pylori, p. 19-28. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and Gastroduodenal Disease, 2 ed. Blackwell Scientific Publications, Oxford. 159. Tytgat, G., and M. Dixon. 1993. Overview: Role in peptic ulcer disease, p. 75-87. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston. |
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