Helicobacter pylori and Schistosoma japonicum co-infection in a Chinese population: helminth infection alters humoral responses to H. pylori and serum pepsinogen I/II ratio

Du, Yiqi; Agnew, Alison; Ye, Xiaoping; Robinson, Philip A.; Forman, David; Crabtree, Jean E.

doi:10.1016/j.micinf.2005.05.017

Cited by 45 publications

(37 citation statements)

References 51 publications

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“…This was coupled with a reduced Th1 response concomitant with higher levels of Th2 cytokines (98). One study of a Chinese population reported that concurrent helminth infections modified serological IgG responses to H. pylori and that this was associated with a decreased risk of developing H. pylori-induced atrophy, as determined by the pepsinogen I/II ratio (75). Similar results were reported in a study of Colombian children, where a higher Th2-associated IgG1 response was reported for children infected with both helminths and H. pylori and living in a coastal region where the incidence of gastric cancer is low (334).…”

Section: Helminth Infectionmentioning

confidence: 99%

Helicobacter pyloriand Gastric Cancer: Factors That Modulate Disease Risk

Wroblewski¹,

2010

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SUMMARY Helicobacter pylori is a gastric pathogen that colonizes approximately 50% of the world's population. Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. Infection with H. pylori is the strongest known risk factor for gastric cancer, which is the second leading cause of cancer-related deaths worldwide. Once H. pylori colonizes the gastric environment, it persists for the lifetime of the host, suggesting that the host immune response is ineffective in clearing this bacterium. In this review, we discuss the host immune response and examine other host factors that increase the pathogenic potential of this bacterium, including host polymorphisms, alterations to the apical-junctional complex, and the effects of environmental factors. In addition to host effects and responses, H. pylori strains are genetically diverse. We discuss the main virulence determinants in H. pylori strains and the correlation between these and the diverse clinical outcomes following H. pylori infection. Since H. pylori inhibits the gastric epithelium of half of the world, it is crucial that we continue to gain understanding of host and microbial factors that increase the risk of developing more severe clinical outcomes.

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Section: Helminth Infectionmentioning

confidence: 99%

Helicobacter pyloriand Gastric Cancer: Factors That Modulate Disease Risk

Wroblewski¹,

2010

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“…Investigators have, however, continued to investigate the effects of helminth coinfections upon H. pylori induced diseases. Schistosoma japonicum infection altered the immunoglobulin G (IgG) serological responses to H. pylori in a Chinese population, and this was associated with less gastric atrophy as measured by pepsinogen I/II ratio [61 ]. Whary et al [62] also demonstrated a higher Th2-associated IgG1 response to H. pylori in Colombian children coinfected with helminths in an area of the country where gastric cancer is rare.…”

Section: Environmental Factorsmentioning

confidence: 99%

Helicobacter pylori and gastric cancer

Pritchard

2006

Current Opinion in Gastroenterology

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“…Furthermore, individuals infected with H. pylori and Schistosoma mansoni have been found to have reduced numbers of apoptotic gastric epithelial cells and decreased gastric epithelial cell proliferation as compared with persons infected with just H. pylori (80). Individuals infected with H. pylori and Schistosoma japonicum also had a substantially higher pepsinogen I/II ratio (a surrogate biomarker for gastric atrophy), indicating that the parasitic infection had a protective effect on progression to atrophy (81). Although other factors, such as life expectancy, diet, limited cancer registries, and limited diagnostic capabilities, are probably important, parasitic coinfection is likely to be strongly protective against gastric cancer development.…”

Section: Host Factors That Affect the Development Of Gastric Cancer Gmentioning

confidence: 99%

Inflammation, atrophy, and gastric cancer

Fox

Wang²

2007

J. Clin. Invest.

691

626

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The association between chronic inflammation and cancer is now well established. This association has recently received renewed interest with the recognition that microbial pathogens can be responsible for the chronic inflammation observed in many cancers, particularly those originating in the gastrointestinal system. A prime example is Helicobacter pylori, which infects 50% of the world's population and is now known to be responsible for inducing chronic gastric inflammation that progresses to atrophy, metaplasia, dysplasia, and gastric cancer. This Review provides an overview of recent progress in elucidating the bacterial properties responsible for colonization of the stomach, persistence in the stomach, and triggering of inflammation, as well as the host factors that have a role in determining whether gastritis progresses to gastric cancer. We also discuss how the increased understanding of the relationship between inflammation and gastric cancer still leaves many questions unanswered regarding recommendations for prevention and treatment.

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Helicobacter pylori and Schistosoma japonicum co-infection in a Chinese population: helminth infection alters humoral responses to H. pylori and serum pepsinogen I/II ratio

Cited by 45 publications

References 51 publications

Helicobacter pyloriand Gastric Cancer: Factors That Modulate Disease Risk

Helicobacter pyloriand Gastric Cancer: Factors That Modulate Disease Risk

Helicobacter pylori and gastric cancer

Inflammation, atrophy, and gastric cancer

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