Immune evasion strategies used by<i>Helicobacter pylori</i>

Lina, Taslima T.; Alzahrani, Shatha; Gonzalez, Jazmin; Pinchuk, Irina V.; Beswick, Ellen J.; Reyes, Victor E.

doi:10.3748/wjg.v20.i36.12753

Cited by 103 publications

(136 citation statements)

References 113 publications

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“…The triggers for transition from transient or latent infection to clinical illness are also unknown and are likely related to environmental and host genetic factors. A similar phenomena is seen in other chronic infectious diseases in humans such as tuberculosis [66], syphilis [78], and H. pylori gastritis [79]. …”

Section: Map and Susceptibilitysupporting

confidence: 68%

Mycobacterium paratuberculosis as a cause of Crohn’s disease

McNees

Markesich

Zayyani

et al. 2015

Expert Review of Gastroenterology & Hepatology

127

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SUMMARY Crohn's disease is a chronic inflammatory bowel disease of unknown cause, affecting approximately 1.4 million North American people. Due to the similarities between Crohn's disease and Johne’s disease, a chronic enteritis in ruminant animals caused by Mycobacterium avium paratuberculosis (MAP) infection, MAP has long been considered to be a potential cause of Crohn's disease. MAP is an obligate intracellular pathogen that cannot replicate outside of animal hosts. MAP is widespread in dairy cattle and because of environmental contamination and resistance to pasteurization and chlorination, humans are frequently exposed through contamination of food and water. MAP can be cultured from the peripheral mononuclear cells from 50 to 100% of patients with Crohn's disease, and less frequently from healthy individuals. Association does not prove causation. We discuss the current data regarding MAP as a potential cause of Crohn's disease and outline what data will be required to firmly prove or disprove the hypothesis.

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Section: Map and Susceptibilitysupporting

confidence: 68%

Mycobacterium paratuberculosis as a cause of Crohn’s disease

McNees

Markesich

Zayyani

et al. 2015

Expert Review of Gastroenterology & Hepatology

127

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“…We and others have shown that deacetylation of peptidoglycan allows H. pylori to evade host clearance (5,25-27). Thus, H. pylori has evolved to express an array of diverse phenotypes to subvert obstacles presented by the host (28), and the ability of H. pylori to alter cagY genotypes is yet another mechanism within the repertoire of this organism to evade host defenses.…”

Section: Discussionmentioning

confidence: 99%

Genetic Manipulation of Helicobacter pylori Virulence Function by Host Carcinogenic Phenotypes

et al. 2017

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Helicobacter pylori is the strongest risk factor for gastric adenocarcinoma, yet only a minority of infected persons ever develop this malignancy. One cancer-linked locus is the cag type 4 secretion system (cagT4SS), which translocates an oncoprotein into host cells. A structural component of the cagT4SS is CagY, which become rapidly altered during in vivo adaptation in mice and rhesus monkeys, rendering the cagT4SS nonfunctional; however, these models rarely develop gastric cancer. We previously demonstrated that the H. pylori cag+ strain 7.13 rapidly induces gastric cancer in Mongolian gerbils. We now use this model, in conjunction with samples from patients with premalignant lesions, to define the effects of a carcinogenic host environment on the virulence phenotype of H. pylori to understand how only a subset of infected individuals develop cancer. H. pylori cagY sequence differences and cagT4SS function were directly related to the severity of inflammation in human gastric mucosa in either a synchronous or metachronous manner. Serial infections of Mongolian gerbils with H. pylori strain 7.13 identified an oscillating pattern of cagT4SS function. The development of dysplasia or cancer selected for attenuated virulence phenotypes, but robust cagT4SS function could be restored upon infection of new hosts. Changes in the genetic composition of cagY mirrored cagT4SS function, although the mechanisms of cagY alterations differed in human isolates (mutations) versus gerbil isolates (addition/deletion of motifs). These results indicate that host carcinogenic phenotypes modify cagT4SS function via altering cagY, allowing the bacteria to persist and induce carcinogenic consequences in the gastric niche.

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“…T. gondii is also found worldwide with prevalence in adult populations ranging from 10% - 80% (Yolken & Torrey, 2008). H. pylori is a bacterium that colonizes the mucosal layer of the gastric epithelium (stomach) and generates a state of chronic inflammation (Lina et al, 2014). Persistent infection with H. pylori causes gastritis, peptic ulcer disease and is associated with other gastric conditions, such as cancer (Lina et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

Early life socioeconomic position and immune response to persistent infections among elderly Latinos

Meier

Haan

Leon

et al. 2016

Social Science & Medicine

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Persistent infections, such as cytomegalovirus (CMV), herpes simplex virus-1 (HSV-1), Helicobacter pylori (H. pylori), and Toxoplasma gondii (T. gondii), are common in the U.S. but their prevalence varies by socioeconomic status. It is unclear if early or later life socioeconomic position (SEP) is a more salient driver of disparities in immune control of these infections. Using data from the Sacramento Area Latino Study on Aging, we examined whether early or later life SEP was the strongest predictor of immune control later in life by contrasting two life course models, the critical period model and the chain of risk model. Early life SEP was measured as a latent variable, derived from parental education and occupation, and food availability. Indicators for SEP in later life included education level and occupation. Individuals were categorized by immune response to each pathogen (seronegative, low, medium and high) with increasing immune response representing poorer immune control. Cumulative immune response was estimated using a latent profile analysis with higher total immune response representing poorer immune control. Structural equation models were used to examine direct, indirect and total effects of early life SEP on each infection and cumulative immune response, controlling for age and gender. The direct effect of early life SEP on immune response was not statistically significant for the infections or cumulative immune response. Higher early life SEP was associated with lower immune response for T. gondii, H. pylori and cumulative immune response through pathways mediated by later life SEP. For CMV, higher early life SEP was both directly associated and partially mediated by later life SEP. No association was found between SEP and HSV-1. Findings from this study support a chain of risk model, whereby early life SEP acts through later life SEP to affect immune response to persistent infections in older age.

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Immune evasion strategies used byHelicobacter pylori

Cited by 103 publications

References 113 publications

Mycobacterium paratuberculosis as a cause of Crohn’s disease

Mycobacterium paratuberculosis as a cause of Crohn’s disease

Genetic Manipulation of Helicobacter pylori Virulence Function by Host Carcinogenic Phenotypes

Early life socioeconomic position and immune response to persistent infections among elderly Latinos

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