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  1. Article: Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development.

    Wroblewski, Lydia E / Peek, Richard M

    Current topics in microbiology and immunology

    2024  Volume 444, Page(s) 25–52

    Abstract: The human pathogen Helicobacter pylori is the strongest known risk factor for gastric disease and cancer, and gastric cancer remains a leading cause of cancer-related death across the globe. Carcinogenic mechanisms associated with H. pylori are ... ...

    Abstract The human pathogen Helicobacter pylori is the strongest known risk factor for gastric disease and cancer, and gastric cancer remains a leading cause of cancer-related death across the globe. Carcinogenic mechanisms associated with H. pylori are multifactorial and are driven by bacterial virulence constituents, host immune responses, environmental factors such as iron and salt, and the microbiota. Infection with strains that harbor the cytotoxin-associated genes (cag) pathogenicity island, which encodes a type IV secretion system (T4SS) confer increased risk for developing more severe gastric diseases. Other important H. pylori virulence factors that augment disease progression include vacuolating cytotoxin A (VacA), specifically type s1m1 vacA alleles, serine protease HtrA, and the outer-membrane adhesins HopQ, BabA, SabA and OipA. Additional risk factors for gastric cancer include dietary factors such as diets that are high in salt or low in iron, H. pylori-induced perturbations of the gastric microbiome, host genetic polymorphisms, and infection with Epstein-Barr virus. This chapter discusses in detail host factors and how H. pylori virulence factors augment the risk of developing gastric cancer in human patients as well as how the Mongolian gerbil model has been used to define mechanisms of H. pylori-induced inflammation and cancer.
    MeSH term(s) Humans ; Stomach Neoplasms/genetics ; Epstein-Barr Virus Infections ; Herpesvirus 4, Human ; Cytotoxins ; Helicobacter pylori/genetics ; Iron ; Virulence Factors/genetics
    Chemical Substances Cytotoxins ; Iron (E1UOL152H7) ; Virulence Factors
    Language English
    Publishing date 2024-01-18
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 210099-X
    ISSN 0070-217X
    ISSN 0070-217X
    DOI 10.1007/978-3-031-47331-9_2
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  2. Article ; Online: Helicobacter pylori: a stealth assassin.

    Wroblewski, Lydia E / Peek, Richard M

    Trends in cancer

    2021  Volume 7, Issue 9, Page(s) 807–808

    Abstract: Helicobacter pylori is a pathogen that confers the highest known risk for gastric cancer. Research directed at understanding the pathogenesis of H. pylori is crucial to identify colonized persons that may subsequently develop neoplasia. Imai et al. ... ...

    Abstract Helicobacter pylori is a pathogen that confers the highest known risk for gastric cancer. Research directed at understanding the pathogenesis of H. pylori is crucial to identify colonized persons that may subsequently develop neoplasia. Imai et al. describe how H. pylori elicits BRCAness and endows epithelial cells with the ability to evade apoptosis.
    MeSH term(s) Antigens, Bacterial ; Bacterial Proteins ; Epithelial Cells ; Gastric Mucosa ; Helicobacter pylori
    Chemical Substances Antigens, Bacterial ; Bacterial Proteins
    Language English
    Publishing date 2021-06-09
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2852626-0
    ISSN 2405-8025 ; 2405-8033 ; 2405-8033
    ISSN (online) 2405-8025 ; 2405-8033
    ISSN 2405-8033
    DOI 10.1016/j.trecan.2021.05.007
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  3. Article ; Online: Helicobacter pylori: Pathogenic enablers - toxic relationships in the stomach.

    Wroblewski, Lydia E / Peek, Richard M

    Nature reviews. Gastroenterology & hepatology

    2016  Volume 13, Issue 6, Page(s) 317–318

    MeSH term(s) Helicobacter Infections ; Helicobacter pylori ; Humans ; Stomach ; Stomach Neoplasms
    Language English
    Publishing date 2016
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2493722-8
    ISSN 1759-5053 ; 1759-5045
    ISSN (online) 1759-5053
    ISSN 1759-5045
    DOI 10.1038/nrgastro.2016.68
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  4. Article ; Online: IL-17RA-Mediated Epithelial Cell Activity Prevents Severe Inflammatory Response to Helicobacter pylori Infection.

    Brackman, Lee C / Jung, Matthew S / Ogaga, Eseoghene I / Joshi, Nikhita / Wroblewski, Lydia E / Piazuelo, M Blanca / Peek, Richard M / Choksi, Yash A / Algood, Holly M Scott

    ImmunoHorizons

    2024  Volume 8, Issue 4, Page(s) 339–353

    Abstract: Helicobacter pylori is a Gram-negative pathogen that colonizes the stomach, induces inflammation, and drives pathological changes in the stomach tissue, including gastric cancer. As the principal cytokine produced by Th17 cells, IL-17 mediates protective ...

    Abstract Helicobacter pylori is a Gram-negative pathogen that colonizes the stomach, induces inflammation, and drives pathological changes in the stomach tissue, including gastric cancer. As the principal cytokine produced by Th17 cells, IL-17 mediates protective immunity against pathogens by inducing the activation and mobilization of neutrophils. Whereas IL-17A is largely produced by lymphocytes, the IL-17 receptor is expressed in epithelial cells, fibroblasts, and hematopoietic cells. Loss of the IL-17RA in mice results in impaired antimicrobial responses to extracellular bacteria. In the context of H. pylori infection, this is compounded by extensive inflammation in Il17ra-/- mice. In this study, Foxa3creIl17rafl/fl (Il17raΔGI-Epi) and Il17rafl/fl (control) mice were used to test the hypothesis that IL-17RA signaling, specifically in epithelial cells, protects against severe inflammation after H. pylori infection. The data indicate that Il17raΔGI-Epi mice develop increased inflammation compared with controls. Despite reduced Pigr expression, levels of IgA increased in the gastric wash, suggesting significant increase in Ag-specific activation of the T follicular helper/B cell axis. Gene expression analysis of stomach tissues indicate that both acute and chronic responses are significantly increased in Il17raΔGI-Epi mice compared with controls. These data suggest that a deficiency of IL-17RA in epithelial cells is sufficient to drive chronic inflammation and hyperactivation of the Th17/T follicular helper/B cell axis but is not required for recruitment of polymorphonuclear neutrophils. Furthermore, the data suggest that fibroblasts can produce chemokines in response to IL-17 and may contribute to H. pylori-induced inflammation through this pathway.
    MeSH term(s) Animals ; Mice ; Epithelial Cells/metabolism ; Helicobacter Infections/immunology ; Helicobacter pylori ; Inflammation/metabolism ; Interleukin-17/metabolism ; Receptors, Interleukin-17/genetics ; Receptors, Interleukin-17/metabolism
    Chemical Substances Interleukin-17 ; Receptors, Interleukin-17 ; Il17ra protein, mouse
    Language English
    Publishing date 2024-04-19
    Publishing country United States
    Document type Journal Article
    ISSN 2573-7732
    ISSN (online) 2573-7732
    DOI 10.4049/immunohorizons.2300078
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  5. Article: Helicobacter pylori, Cancer, and the Gastric Microbiota.

    Wroblewski, Lydia E / Peek, Richard M

    Advances in experimental medicine and biology

    2016  Volume 908, Page(s) 393–408

    Abstract: Gastric adenocarcinoma is one of the leading causes of cancer-related death worldwide and Helicobacter pylori infection is the strongest known risk factor for this disease. Although the stomach was once thought to be a sterile environment, it is now ... ...

    Abstract Gastric adenocarcinoma is one of the leading causes of cancer-related death worldwide and Helicobacter pylori infection is the strongest known risk factor for this disease. Although the stomach was once thought to be a sterile environment, it is now known to house many bacterial species leading to a complex interplay between H. pylori and other residents of the gastric microbiota. In addition to the role of H. pylori virulence factors, host genetic polymorphisms, and diet, it is now becoming clear that components of the gastrointestinal microbiota may also influence H. pylori-induced pathogenesis. In this chapter, we discuss emerging data regarding the gastric microbiota in humans and animal models and alterations that occur to the composition of the gastric microbiota in the presence of H. pylori infection that may augment the risk of developing gastric cancer.
    MeSH term(s) Animals ; Gastrointestinal Microbiome/physiology ; Genetic Predisposition to Disease/genetics ; Helicobacter Infections/genetics ; Helicobacter Infections/microbiology ; Helicobacter Infections/pathology ; Helicobacter pylori/pathogenicity ; Helicobacter pylori/physiology ; Host-Pathogen Interactions ; Humans ; Stomach/metabolism ; Stomach/microbiology ; Stomach/pathology ; Stomach Neoplasms/genetics ; Stomach Neoplasms/microbiology ; Stomach Neoplasms/pathology ; Virulence
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-3-319-41388-4_19
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  6. Article ; Online: Helicobacter pylori

    Dooyema, Samuel D R / Noto, Jennifer M / Wroblewski, Lydia E / Piazuelo, M Blanca / Krishna, Uma / Suarez, Giovanni / Romero-Gallo, Judith / Delgado, Alberto G / Peek, Richard M

    Gut microbes

    2022  Volume 14, Issue 1, Page(s) 2105102

    Abstract: Chronic mucosal pathogens have evolved multiple strategies to manipulate the host immune response; consequently, microbes contribute to the development of >2 million cases of cancer/year. Gastric adenocarcinoma is the fourth leading cause of cancer- ... ...

    Abstract Chronic mucosal pathogens have evolved multiple strategies to manipulate the host immune response; consequently, microbes contribute to the development of >2 million cases of cancer/year. Gastric adenocarcinoma is the fourth leading cause of cancer-related death and
    MeSH term(s) Animals ; Gastric Mucosa/metabolism ; Gastrointestinal Microbiome ; Helicobacter Infections/microbiology ; Helicobacter pylori/genetics ; Immunity, Innate ; Inflammation/metabolism ; Mice ; Nucleic Acids/metabolism ; Stomach Neoplasms/microbiology
    Chemical Substances Nucleic Acids
    Language English
    Publishing date 2022-07-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2575755-6
    ISSN 1949-0984 ; 1949-0984
    ISSN (online) 1949-0984
    ISSN 1949-0984
    DOI 10.1080/19490976.2022.2105102
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  7. Article ; Online: The Role of the Microbiome in Gastrointestinal Cancer.

    Wroblewski, Lydia E / Peek, Richard M / Coburn, Lori A

    Gastroenterology clinics of North America

    2016  Volume 45, Issue 3, Page(s) 543–556

    Abstract: Humans are host to complex microbial communities previously termed normal flora and largely overlooked. However, resident microbes contribute to both health and disease. Investigators are beginning to define microbes that contribute to the development of ...

    Abstract Humans are host to complex microbial communities previously termed normal flora and largely overlooked. However, resident microbes contribute to both health and disease. Investigators are beginning to define microbes that contribute to the development of gastrointestinal malignancies and the mechanisms by which this occurs. Resident microbes can induce inflammation, leading to cell proliferation and altered stem cell dynamics, which can lead to alterations in DNA integrity and immune regulation and promote carcinogenesis. Studies in human patients and rodent models of cancer have identified alterations in the microbiota of the stomach, esophagus, and colon that increase the risk for malignancy.
    MeSH term(s) Adenocarcinoma/immunology ; Adenocarcinoma/microbiology ; Animals ; Carcinogenesis/immunology ; Cell Proliferation ; Colonic Polyps/immunology ; Colonic Polyps/microbiology ; Colorectal Neoplasms/immunology ; Colorectal Neoplasms/microbiology ; Diet ; Disease Models, Animal ; Esophageal Neoplasms/immunology ; Esophageal Neoplasms/microbiology ; Gastrointestinal Microbiome ; Gastrointestinal Neoplasms/immunology ; Gastrointestinal Neoplasms/microbiology ; Gastrointestinal Tract/immunology ; Gastrointestinal Tract/microbiology ; Helicobacter Infections/immunology ; Helicobacter Infections/microbiology ; Helicobacter pylori ; Humans ; Inflammation/immunology ; Inflammation/microbiology ; Microbiota ; Stem Cells ; Stomach Neoplasms/immunology ; Stomach Neoplasms/microbiology
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 92114-2
    ISSN 1558-1942 ; 0889-8553
    ISSN (online) 1558-1942
    ISSN 0889-8553
    DOI 10.1016/j.gtc.2016.04.010
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  8. Article ; Online: Helicobacter pylori in gastric carcinogenesis: mechanisms.

    Wroblewski, Lydia E / Peek, Richard M

    Gastroenterology clinics of North America

    2013  Volume 42, Issue 2, Page(s) 285–298

    Abstract: Helicobacter pylori infection induces chronic inflammation and is the strongest known risk factor for gastric cancer. The genomes of H pylori are highly diverse and therefore bacterial virulence factors play an important role in determining the outcome ... ...

    Abstract Helicobacter pylori infection induces chronic inflammation and is the strongest known risk factor for gastric cancer. The genomes of H pylori are highly diverse and therefore bacterial virulence factors play an important role in determining the outcome of H pylori infection, in combination with host responses that are augmented by environmental and dietary risk factors. It is important to gain further understanding of the pathogenesis of H pylori infection to develop more effective treatments for this common but deadly malignancy. This review focuses on the specific mechanisms used by H pylori to drive gastric carcinogenesis.
    MeSH term(s) Antigens, Bacterial/genetics ; Antigens, Bacterial/metabolism ; Bacterial Outer Membrane Proteins/genetics ; Bacterial Outer Membrane Proteins/metabolism ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Carcinogenesis/genetics ; Carcinogenesis/immunology ; Carcinogenesis/pathology ; Helicobacter Infections/complications ; Helicobacter Infections/immunology ; Helicobacter pylori ; Humans ; Stomach Neoplasms/microbiology ; Stomach Neoplasms/pathology ; Virulence Factors/genetics ; Virulence Factors/metabolism
    Chemical Substances Antigens, Bacterial ; Bacterial Outer Membrane Proteins ; Bacterial Proteins ; VacA protein, Helicobacter pylori ; Virulence Factors ; cagA protein, Helicobacter pylori
    Language English
    Publishing date 2013-03-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 92114-2
    ISSN 1558-1942 ; 0889-8553
    ISSN (online) 1558-1942
    ISSN 0889-8553
    DOI 10.1016/j.gtc.2013.01.006
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  9. Article ; Online: When guests simply will not leave.

    Wroblewski, Lydia E / Peek, Richard M

    Cell host & microbe

    2012  Volume 12, Issue 6, Page(s) 733–734

    Abstract: Chronic pathogens have evolved exquisite mechanisms of self-regulation via manipulation of host signaling pathways; however, pathologic consequences may ensue. Tsugawa et al. (2012) now report a mechanism of checks and balances used by Helicobacter ... ...

    Abstract Chronic pathogens have evolved exquisite mechanisms of self-regulation via manipulation of host signaling pathways; however, pathologic consequences may ensue. Tsugawa et al. (2012) now report a mechanism of checks and balances used by Helicobacter pylori that is undermined by gastric stem cells, which may lower the threshold for gastric cancer.
    MeSH term(s) Antigens, Bacterial/metabolism ; Bacterial Proteins/metabolism ; Helicobacter pylori/pathogenicity ; Humans ; Reactive Oxygen Species/immunology ; Virulence Factors/metabolism ; Volition
    Chemical Substances Antigens, Bacterial ; Bacterial Proteins ; Reactive Oxygen Species ; Virulence Factors
    Language English
    Publishing date 2012-12-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2278004-X
    ISSN 1934-6069 ; 1931-3128
    ISSN (online) 1934-6069
    ISSN 1931-3128
    DOI 10.1016/j.chom.2012.11.008
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  10. Article ; Online: "Targeted disruption of the epithelial-barrier by Helicobacter pylori".

    Wroblewski, Lydia E / Peek, Richard M

    Cell communication and signaling : CCS

    2011  Volume 9, Issue 1, Page(s) 29

    Abstract: Helicobacter pylori colonizes the human gastric epithelium and induces chronic gastritis, which can lead to gastric cancer. Through cell-cell contacts the gastric epithelium forms a barrier to protect underlying tissue from pathogenic bacteria; however, ... ...

    Abstract Helicobacter pylori colonizes the human gastric epithelium and induces chronic gastritis, which can lead to gastric cancer. Through cell-cell contacts the gastric epithelium forms a barrier to protect underlying tissue from pathogenic bacteria; however, H. pylori have evolved numerous strategies to perturb the integrity of the gastric barrier. In this review, we summarize recent research into the mechanisms through which H. pylori disrupts intercellular junctions and disrupts the gastric epithelial barrier.
    Language English
    Publishing date 2011-11-01
    Publishing country England
    Document type Journal Article
    ISSN 1478-811X
    ISSN (online) 1478-811X
    DOI 10.1186/1478-811X-9-29
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