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was first described in 1983 by Barry Marshall and Robin Warren, who were awarded a Nobel prize for this work in 2005. infections are extremely common, and approximately half the world’s population have the bacteria in their stomachs. The virulence determinant which confers the most significant increases in the risk of peptic ulcer disease and gastric cancer is the cytotoxin-associated gene pathogenicity island (cag PaI). Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is an uncommon disease, with an incidence of approximately 0.8 per 100,000 per year. Iron deficiency anemia (IDA), the most common form of anemia, is highly prevalent in developing countries, where infection is virtually ubiquitous. Several researchers have reported an association between infection and vitamin B deficiency and malabsorption, even when gastric corpus atrophy is minimal. Chronic infection with has been reported as a possible causal factor in several extragastric diseases, including idiopathic thrombocytopenic purpura (ITP), ischemic heart disease, hepatobiliary disease, pulmonary disease, growth retardation, and Parkinson’s disease. A number of researchers have reported that abrogates the severity of gastroesophageal reflux disease (GERD) and its sequelae, and more recently there has been great interest in the possibility that the infection may help to prevent the development of allergy, asthma, and some autoimmune diseases. From an evolutionary viewpoint, one could consider that when colonization is absent, as is increasingly the case in developed countries, our immunity and gastroesophageal physiology are impaired.

Citation: Robinson K, Atherton J. 2009. , p 107-133. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch7
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Image of Figure 1.
Figure 1.

Host cell signalling events induced by the pathogenicity island. The PaI-encoded type IV secretion system delivers CagA into epithelial cells. CagA is phosphorylated by Scr kinases prior to its interaction with SHP-2, a protein phosphatase. Subsequent activation of MAP kinase pathways results in a number of cellular effects, including actin rearrangements, cellular proliferation and cell scattering, increased apoptosis, disruption of the cell cycle, and the expression of proinflammatory genes. In addition, when the type IV secretion system connects bacterial and epithelial cell cytoplasm, bacterial cell wall components enter the epithelial cell and activate other cell signaling pathways. Peptidoglycan components bind to and activate the intracellular pattern recognition receptor Nod1, leading to activation of NF-κB ( ). This transcription factor stimulates expression of genes encoding factors which attract inflammatory cells (such as IL-8) and genes encoding antibacterial peptides ( ).

Citation: Robinson K, Atherton J. 2009. , p 107-133. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch7
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Image of Figure 2.
Figure 2.

Effects of VacA polymorphisms on cytotoxic activity and associations with disease. The gene varies most in the signal region (which determines cytotoxic activity and may be type s1 or s2), the intermediate region located within the p37 subunit (which determines cytotoxic activity and may be type i1 or i2), and the mid-region within the p58 subunit (which determines binding to host cells and may be type m1 or m2). Only the combinations of regions shown occur commonly.

Citation: Robinson K, Atherton J. 2009. , p 107-133. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch7
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Figure 3.

CD4 T-cell subsets and their associations with -induced inflammation and disease.

Citation: Robinson K, Atherton J. 2009. , p 107-133. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch7
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Figure 4.

Colonization and gastritis patterns in the stomach: their effects on gastric acid production and their associations with duodenal and gastric ulceration.

Citation: Robinson K, Atherton J. 2009. , p 107-133. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch7
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