Helicobacter pylori Chronic Infection Selects for Effective Colonizers of Metaplastic Glands

O’Brien, Valerie P.; Jackson, L K; Frick, Jacob P; Martinez, Armando E Rodriguez; Jones, D S; Johnston, Christopher D; Salama, Nina R.

doi:10.1128/mbio.03116-22

Cited by 5 publications

(5 citation statements)

References 59 publications

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“…According to our findings, the vacA s1i1d1m1c1n1 type is the most prevalent in H. pylori -Mon ( Table S5 ). SabB is a putative adhesin that arose via a gene fusion involving the sialic acid-binding adhesin (SabA) gene [ 50 ]. However, very little is known about the role of this protein.…”

Section: Discussionmentioning

confidence: 99%

“…However, very little is known about the role of this protein. A SabB, according to the findings of one study, may have a role in the changing gastric environment during the development of gastric disease by encouraging bacterial adhesin gene variation linked with increased colonization [ 50 ]. In a meta-analysis of 18 studies, “on” oipA status was associated with higher odds of PUD and GC [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

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Study of Helicobacter pylori Isolated from a High-Gastric-Cancer-Risk Population: Unveiling the Comprehensive Analysis of Virulence-Associated Genes including Secretion Systems, and Genome-Wide Association Study

Saruuljavkhlan,

Alfaray,

Oyuntsetseg

et al. 2023

Cancers

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Background: The prevalence of gastric cancer in Mongolia, in East Asia, remains the highest in the world. However, most Helicobacter pylori strains in Mongolia have a less virulent Western-type CagA. We aimed to determine how H. pylori genomic variation affected gastric diseases, especially gastric cancer, based on comprehensive genome analysis. Methods: We identified a set of 274 virulence-associated genes in H. pylori, including virulence factor and outer membrane protein (OMP) genes, the type four secretion system gene cluster, and 13 well-known virulence gene genotypes in 223 H. pylori strains and their associations with gastric cancer and other gastric diseases. We conducted a genome-wide association study on 158 H. pylori strains (15 gastric cancer and 143 non-gastric cancer strains). Results: Out of 274 genes, we found 13 genes were variable depending on disease outcome, especially iron regulating OMP genes. H. pylori strains from Mongolia were divided into two main subgroups: subgroup (Sg1) with high risk and Sg2 with low risk for gastric cancer. The general characteristics of Sg1 strains are that they possess more virulence genotype genes. We found nine non-synonymous single nucleotide polymorphisms in seven genes that are linked with gastric cancer strains. Conclusions: Highly virulent H. pylori strains may adapt through host-influenced genomic variations, potentially impacting gastric carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Study of Helicobacter pylori Isolated from a High-Gastric-Cancer-Risk Population: Unveiling the Comprehensive Analysis of Virulence-Associated Genes including Secretion Systems, and Genome-Wide Association Study

Saruuljavkhlan,

Alfaray,

Oyuntsetseg

et al. 2023

Cancers

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“…The antrum contains gastrin-secreting G cells that stimulate gastric acid secretion and somatostatin-secreting D cells that inhibit gastric acid secretion ( 26 ). Previous studies have shown that H. pylori preferentially colonizes the antrum at early stages of infection, leading to antral inflammation ( 27 , 28 ). H. pylori- induced atrophic gastritis (characterized by a loss of parietal and chief cells from the corpus) can develop over the course of infection, typically beginning in the antrocorporal transitional mucosa (the junction between the antrum and the corpus) and spreading proximally along the lesser curvature of the stomach ( 29 ).…”

Section: Introductionmentioning

confidence: 99%

Remodeling of the gastric environment in Helicobacter pylori -induced atrophic gastritis

Shuman,

Lin,

Westland

et al. 2024

mSystems

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Helicobacter pylori colonization of the human stomach is a strong risk factor for gastric cancer. To investigate H. pylori -induced gastric molecular alterations, we used a Mongolian gerbil model of gastric carcinogenesis. Histologic evaluation revealed varying levels of atrophic gastritis (a premalignant condition characterized by parietal and chief cell loss) in H. pylori -infected animals, and transcriptional profiling revealed a loss of markers for these cell types. We then assessed the spatial distribution and relative abundance of proteins in the gastric tissues using imaging mass spectrometry and liquid chromatography with tandem mass spectrometry. We detected striking differences in the protein content of corpus and antrum tissues. Four hundred ninety-two proteins were preferentially localized to the corpus in uninfected animals. The abundance of 91 of these proteins was reduced in H. pylori -infected corpus tissues exhibiting atrophic gastritis compared with infected corpus tissues exhibiting non-atrophic gastritis or uninfected corpus tissues; these included numerous proteins with metabolic functions. Fifty proteins localized to the corpus in uninfected animals were diffusely delocalized throughout the stomach in infected tissues with atrophic gastritis; these included numerous proteins with roles in protein processing. The corresponding alterations were not detected in animals infected with a H. pylori ∆ cagT mutant (lacking Cag type IV secretion system activity). These results indicate that H. pylori can cause loss of proteins normally localized to the gastric corpus as well as diffuse delocalization of corpus-specific proteins, resulting in marked changes in the normal gastric molecular partitioning into distinct corpus and antrum regions. IMPORTANCE A normal stomach is organized into distinct regions known as the corpus and antrum, which have different functions, cell types, and gland architectures. Previous studies have primarily used histologic methods to differentiate these regions and detect H. pylori -induced alterations leading to stomach cancer. In this study, we investigated H. pylori -induced gastric molecular alterations in a Mongolian gerbil model of carcinogenesis. We report the detection of numerous proteins that are preferentially localized to the gastric corpus but not the antrum in a normal stomach. We show that stomachs with H. pylori- induced atrophic gastritis (a precancerous condition characterized by the loss of specialized cell types) exhibit marked changes in the abundance and localization of proteins normally localized to the gastric corpus. These results provide new insights into H. pylori -induced gastric molecular alterations that are associated with the development of stomach cancer.

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“…4 The incidence of gastric cancer attributable to H. pylori infection is approximately 75%. 5 H. pylori often infects individuals during childhood and can persist in the gastric mucosa for life in the absence of eradication therapy. 6 Chronic infection with H. pylori exposes the gastric mucosa to various bacterial components such as lipopolysaccharide (LPS), outer membrane vesicles (OMVs), and toxic proteins.…”

Section: Introductionmentioning

confidence: 99%

“…Studies show that the infection rate of H. pylori is remarkably high (90%) in patients with atrophic gastritis and intestinal metaplasia 4 . The incidence of gastric cancer attributable to H. pylori infection is approximately 75% 5 . H. pylori often infects individuals during childhood and can persist in the gastric mucosa for life in the absence of eradication therapy 6 …”

Section: Introductionmentioning

confidence: 99%

The role of toll‐like receptors in immune tolerance induced by Helicobacter pylori infection

Zhang,

Yan

et al. 2023

Helicobacter

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Helicobacter pylori (H. pylori) is a gram‐negative, microaerobic bacterium that colonizes the gastric mucosa in about half of the world's population. H. pylori infection can lead to various diseases. Chronic infection by H. pylori exposes the gastric mucosa to bacterial components such as lipopolysaccharide (LPS), outer membrane vesicles (OMVs), and several toxic proteins. Infected with H. pylori activates the release of pro‐inflammatory factors and triggers inflammatory responses that damage the gastric mucosa. As the only microorganism that permanently colonizes the human stomach, H. pylori can suppress host immunity to achieve long‐term colonization. Toll‐like receptors (TLRs) play a crucial role in T‐cell activation, promoting innate immune responses and immune tolerance during H. pylori infection. Among the 10 TLRs found in humans, TLR2, TLR4, TLR5, and TLR9 have been thoroughly investigated in relation to H. pylori‐linked immune regulation. In the present review, we provide a comprehensive analysis of the various mechanisms employed by different TLRs in the induction of immune tolerance upon H. pylori infection, which will contribute to the research of pathogenic mechanism of H. pylori.

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Helicobacter pylori Chronic Infection Selects for Effective Colonizers of Metaplastic Glands

Abstract: Chronic infection with Helicobacter pylori is the primary risk factor for developing stomach cancer. As disease progresses H. pylori must adapt to a changing host tissue environment that includes induction of new cell fates in the cells that line the stomach.

Cited by 5 publications

References 59 publications

Study of Helicobacter pylori Isolated from a High-Gastric-Cancer-Risk Population: Unveiling the Comprehensive Analysis of Virulence-Associated Genes including Secretion Systems, and Genome-Wide Association Study

Study of Helicobacter pylori Isolated from a High-Gastric-Cancer-Risk Population: Unveiling the Comprehensive Analysis of Virulence-Associated Genes including Secretion Systems, and Genome-Wide Association Study

Remodeling of the gastric environment in Helicobacter pylori -induced atrophic gastritis

The role of toll‐like receptors in immune tolerance induced by Helicobacter pylori infection

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