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Mechanisms of Helicobacter pylori Infection: Bacterial Factors

  • Chapter
Gastroduodenal Disease and Helicobacter pylori

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 241))

Abstract

The pathogenesis of Helicobacter pylori can be described in three steps: (a) gain of entry and colonization of the unique niche of the human gastric mucosa; (b) avoidance, subversion, or exploitation of the nonspecific and specific human immune system; and (c) multiplication, tissue damage, and transmission to a new susceptible host or spread to adjacent tissue (Falkow 1991, 1997) (Fig. 1). A virulence factor is a gene product involved in one or more of these steps. To properly assess whether a particular gene is involved in virulence, the candidate gene must be cloned, disrupted in H. pylori and be shown to have reduced virulence in an appropriate animal model. This is best determined by testing the interaction of H. pylori with human gastric epithelial cells or phagocytic cells or by assessment of infection in H. pylori animal models. Finally, “molecular Koch’s postulates” (Falkow 1988) can be completed by cloning the wild-type gene into a shuttle plasmid, which should then complement the H. pylori chromosomal defect, resulting in recovery of virulence.

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McGee, D.J., Mobley, H.L.T. (1999). Mechanisms of Helicobacter pylori Infection: Bacterial Factors. In: Westblom, T.U., Czinn, S.J., Nedrud, J.G. (eds) Gastroduodenal Disease and Helicobacter pylori . Current Topics in Microbiology and Immunology, vol 241. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60013-5_9

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