The paradox of <i>Helicobacter pylori</i>: how does <i>H. pylori</i> infection protect against esophageal cancer?

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Abstract

Helicobacter pylori is a microaerophilic gram-negative bacterium infecting around half of the world’s population. Despite its well-known role in gastric malignancies, its impact on esophageal cancer comes with a complex paradox. Several mechanisms have been proposed to explain its observed lack of carcinogenic activity in the esophagus, including the trigger of anti-inflammatory pathways, promoting atrophic gastritis, and esophageal microbiome modulation. However, recent studies have highlighted a significantly more complicated interplay, where H. pylori, typically considered a pathogen, may even deliver a protective effect against esophageal carcinogenesis. This paper aims to evaluate the prevalence of H. pylori infection among patients with esophageal carcinoma, discussing the underlying mechanisms of the paradoxical effects of H. pylori on esophageal cancer.

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Helicobacter pylori and gastric cancer: factors that modulate disease risk.

Lydia E Wroblewski, Richard M Peek, Keith T Wilson (2010)

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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Helicobacter pylori infection

Peter Malfertheiner, M Constanza Camargo, Emad Munir El-Omar … (2023)

Helicobacter pylori infection causes chronic gastritis, which can progress to severe gastroduodenal pathologies, including peptic ulcer, gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma. H. pylori is usually transmitted in childhood and persists for life if untreated. The infection affects around half of the population in the world but prevalence varies according to location and sanitation standards. H. pylori has unique properties to colonize gastric epithelium in an acidic environment. The pathophysiology of H. pylori infection is dependent on complex bacterial virulence mechanisms and their interaction with the host immune system and environmental factors, resulting in distinct gastritis phenotypes that determine possible progression to different gastroduodenal pathologies. The causative role of H. pylori infection in gastric cancer development presents the opportunity for preventive screen-and-treat strategies. Invasive, endoscopy-based and non-invasive methods, including breath, stool and serological tests, are used in the diagnosis of H. pylori infection. Their use depends on the specific individual patient history and local availability. H. pylori treatment consists of a strong acid suppressant in various combinations with antibiotics and/or bismuth. The dramatic increase in resistance to key antibiotics used in H. pylori eradication demands antibiotic susceptibility testing, surveillance of resistance and antibiotic stewardship.

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Inflammation and intestinal metaplasia of the distal esophagus are associated with alterations in the microbiome.

Richard Peek, Liying Yang, Fritz Francois … (2009)

Gastroesophageal reflux causes inflammation and intestinal metaplasia and its downstream sequelum adenocarcinoma in the distal esophagus. The incidence of esophageal adenocarcinoma has increased approximately 6-fold in the United States since the 1970s, accompanied with a significant increase in the prevalence of gastroesophageal reflux disease (GERD). Despite extensive epidemiologic study, the cause for GERD and the unexpected increases remain unexplainable. Microbes are among the environmental factors that may contribute to the etiology of GERD, but very little research has been done on the esophageal microbiome, particularly in its relation to GERD. This is the first comprehensive reported correlation between a change in the esophageal microbiome and esophageal diseases. Biopsy samples of the distal esophagus were collected from 34 patients. Host phenotypes were histologically defined as normal, esophagitis, or Barrett's esophagus (intestinal metaplasia). Microbiomes from the biopsy samples were analyzed by bacterial 16S ribosomal RNA gene survey and classified into types using unsupervised cluster analysis and phenotype-guided analyses. Independence between host phenotypes and microbiome types were analyzed by Fisher exact test. Esophageal microbiomes can be classified into 2 types. The type I microbiome was dominated by the genus Streptococcus and concentrated in the phenotypically normal esophagus. Conversely, the type II microbiome contained a greater proportion of gram-negative anaerobes/microaerophiles and primarily correlated with esophagitis (odds ratio, 15.4) and Barrett's esophagus (odds ratio, 16.5). In the human distal esophagus, inflammation and intestinal metaplasia are associated with global alteration of the microbiome. These findings raise the issue of a possible role for dysbiosis in the pathogenesis of reflux-related disorders.

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Author and article information

Contributors

Erfan Banisefid:

ORCID: https://orcid.org/0000-0001-7825-2759

Ehsan Nasiri:

ORCID: https://orcid.org/0000-0002-9679-5623

Seyedyashar Pourebrahimian Leilabadi:

ORCID: https://orcid.org/0009-0006-7127-8052

Sina Hamzehzadeh:

ORCID: https://orcid.org/0000-0001-5344-4885

Mohammad Amin Akbarzadeh:

ORCID: https://orcid.org/0000-0002-9589-104X

Mohammad-Salar Hosseini:

ORCID: https://orcid.org/0000-0003-2765-5018

Journal

Journal ID (nlm-ta): Ann Med Surg (Lond)

Journal ID (iso-abbrev): Ann Med Surg (Lond)

Journal ID (publisher-id): MS9

Title: Annals of Medicine and Surgery

Publisher: Lippincott Williams & Wilkins (Hagerstown, MD )

ISSN (Electronic): 2049-0801

Publication date Collection: December 2024

Publication date (Electronic): 21 October 2024

Volume: 86

Issue: 12

Pages: 7221-7226

Affiliations

[a ]Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran

[b ]Liver and Gastrointestinal Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

[c ]Medical Philosophy and History Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

[d ]Research Center for Evidence-Based Medicine, Iranian EBM Center: A JBI Center of Excellence, Tabriz University of Medical Sciences, Tabriz, Iran

[e ]Research Center for Integrative Medicine in Aging, Aging Research Institute, Tabriz University of Medical Sciences, Tabriz, Iran

[f ]Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

Author notes

[* ]Corresponding author. Address: Research Center for Integrative Medicine in Aging, Aging Research Institute, Tabriz University of Medical Sciences, Golgasht Street, Tabriz, 51666, East Azerbaijan, Iran. Tel.: +413 336 6581; fax: +413 334 1994. E-mail: hosseini.msalar@ 123456gmail.com , hosseinim@ 123456tbzmed.ac.ir (M.-S. Hosseini).

Author information

Erfan Banisefid https://orcid.org/0000-0001-7825-2759

Ehsan Nasiri https://orcid.org/0000-0002-9679-5623

Seyedyashar Pourebrahimian Leilabadi https://orcid.org/0009-0006-7127-8052

Sina Hamzehzadeh https://orcid.org/0000-0001-5344-4885

Mohammad Amin Akbarzadeh https://orcid.org/0000-0002-9589-104X

Mohammad-Salar Hosseini https://orcid.org/0000-0003-2765-5018

Article

Publisher ID: AMSU-D-24-01744 Accession ID: 00043

DOI: 10.1097/MS9.0000000000002674

PMC ID: 11623814

PubMed ID: 39649904

SO-VID: 6b89693c-633b-4731-b69f-2a100df3a1ff

License:

This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0/

History

Date received : 21 August 2024

Date accepted : 10 October 2024

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Keywords: dysbiosis,esophageal neoplasms,gastrointestinal neoplasms,helicobacter pylori,microbiota

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Keywords: dysbiosis, esophageal neoplasms, gastrointestinal neoplasms, helicobacter pylori, microbiota

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The paradox of Helicobacter pylori: how does H. pylori infection protect against esophageal cancer?

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Abstract

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Most cited references 65

Helicobacter pylori and gastric cancer: factors that modulate disease risk.

Helicobacter pylori infection

Inflammation and intestinal metaplasia of the distal esophagus are associated with alterations in the microbiome.

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