Inflammation, DNA Damage, Helicobacter pylori and Gastric Tumorigenesis

Kalisperati, Polyxeni; Spanou, Evangelia; Pateras, Ioannis S.; Korkolopoulou, Penelope; Varvarigou, Anastasia; Karavokyros, Ioannis; Gorgoulis, Vassilis G.; Vlachoyiannopoulos, Panayiotis G.; Sougioultzis, Stavros

doi:10.3389/fgene.2017.00020

Cited by 65 publications

(50 citation statements)

References 104 publications

(119 reference statements)

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“…During H. pylori infection, the adaptive immune response is usually associated with T helper cells (Th‐1 cells and Th‐17 T cells) that induce the secretion of IL‐17 and INFγ after inducing inflammation and cell damage. The impaired modulation of Th‐1 and Th‐17 cells is hypothesized for ongoing or long‐term infection . VacA was primarily identified because of its ability to induce vacuolization of epithelial cells.…”

Section: Ureasementioning

confidence: 98%

“…The impaired modulation of Th-1 and Th-17 cells is hypothesized for ongoing or long-term infection. 107,110 VacA was primarily identified because of its ability to induce vacuolization of epithelial cells. Later on, it has been reported that VacA also inhibits T-cell proliferation by downregulating the level of IL-2.…”

Section: Inhibition Of Th-1-and Th-17-mediated Immunological Responsesmentioning

confidence: 99%

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Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

Gupta

Maurya

Verma

et al. 2019

J of Cellular Biochemistry

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Helicobacter pylori and humans have one of the most complex relationships in nature. How a bacterium manages to live in one of the harshest and hostile environments is a topic of unraveling mysteries. H. pylori is a prevalent species and it colonizes the human gut of more than 50% of the world population. It infects the epithelial region of antrum and persists there for a long period. Over the time of evolution, H. pylori has developed complex strategies to extend the degree of inflammation in gastric mucosa. H. pylori needs specific adaptations for initial colonization into the host environment like helical shape, flagellar movement, chemotaxis, and the production of urease enzyme that neutralizes acidic environment of the stomach. There are several factors from the bacterium as well as from the host that participate in these complex interactions. On the other hand, to establish the persistent infection, H. pylori escapes the immune system by mimicking the host antigens. This pathogen has the ability to dodge the immune system and then persist there in the form of host cell, which leads to immune tolerance. H. pylori has an ability to manipulate its own pathogen‐associated molecular patterns, which leads to an inhibition in the binding with specific pattern recognition receptors of the host to avoid immune cell detection. Also, it manipulates the host metabolic homeostasis in the gastric epithelium. Besides, it has several genes, which may get involved in the acquisition of nutrition from the host to survive longer in the host. Due to the persistence of H. pylori, it causes chronic inflammation and raises the chances of gastric cancer. This review highlights the important elements, which are certainly responsible for the persistence of H. pylori in the human host.

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Section: Ureasementioning

confidence: 98%

Section: Inhibition Of Th-1-and Th-17-mediated Immunological Responsesmentioning

confidence: 99%

Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

Gupta

Maurya

Verma

et al. 2019

J of Cellular Biochemistry

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“…Infection‐related cancer is caused either directly by tumorigenic effects of the pathogen or indirectly through accompanying inflammation and subsequent genomic instability . H pylori has the ability to induce a chronic immune response, including persistent oxidative stress in the stomach, resulting in DNA damage .…”

Section: Dna Damage: a New Perspective To Understand Helicobacter Pylmentioning

confidence: 99%

“…Upon recognition of H pylori , both innate and adaptive host responses are activated during the infection. Neutrophils and macrophages, as well as gastric epithelial cells, trigger ROS and RON production and create oxidative stress . The goal of ROS production by the host cells is to limit the development of pathogens.…”

Section: Dna Damage: a New Perspective To Understand Helicobacter Pylmentioning

confidence: 99%

“…H pylori also induces migration and invasion of GC cells through reduction of E‐cadherin function by activation of MMP‐3 and MMP‐7 . Recent studies have shown that H pylori was predisposed to induce DNA damage, notably double‐strand breaks (DSBs) . Importantly, DSBs are cytotoxic lesions that promote carcinogenesis if they are left unrepaired or are inappropriately repaired …”

Section: Introductionmentioning

confidence: 99%

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A lucid review of Helicobacter pylori‐induced DNA damage in gastric cancer

Xie

2019

Helicobacter

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Helicobacter pylori (H pylori) is the main risk factor for gastric cancer (GC). In recent years, many studies have addressed the effects of H pylori itself and of H pylori-induced chronic inflammation on DNA damage. Unrepaired or inappropriately repaired DNA damage is one possible carcinogenic mechanism. We may conclude that H pylori-induced DNA damage is one of the carcinogenic mechanisms of GC. In this review, we summarize the interactions between H pylori and DNA damage and the effects of H pylori-induced DNA damage on GC. Then, focusing on oxidative stress, we introduce the application of antioxidants in GC. At the end of this review, we discuss the outlook for further research on H pylori-induced DNA damage. K E Y W O R D SDNA damage, Helicobacter pylori, NF-κB, PLK

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The toxic effects of Helicobacter pylori and benzo(a)pyrene in inducing atrophic gastritis and gut microbiota dysbiosis in Mongolian gerbils

Huang,

Chen,

et al. 2024

Food Science & Nutrition

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Food chemical and microbiological contamination are major global food safety issues. This study investigated the combined effects of the food‐borne pathogen Helicobacter pylori (H. pylori) and the pollutant benzo(a)pyrene (Bap) on atrophic gastritis and gut microbiota in Mongolian gerbils. The results demonstrated that simultaneous administration of H. pylori and Bap caused more severe weight loss, DNA damage, and gastritis in Mongolian gerbils compared with those exposed to H. pylori or Bap alone. The combination also significantly increased the serum level of proinflammatory cytokines, including IL‐1β (p < .05), IL‐6 (p < .0001), and TNF‐α (p < .05). Additionally, the H. pylori and Bap combination altered the composition of gut microbiota in Mongolian gerbils: the relative abundance of Lactobacillus and Ligilactobacillus at the genus level (p < .05) was significantly reduced while the relative abundance of Allobaculum and Erysipelotrichaceae enhanced (p < .0001, p < .05). Our study revealed that the synergy of H. pylori and Bap can boost the development of atrophic gastritis and lead to gut microbiota dysbiosis in Mongolian gerbils, which provides essential implications for preventing contaminated foods to sustain life and promote well‐being.

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Inflammation, DNA Damage, Helicobacter pylori and Gastric Tumorigenesis

Cited by 65 publications

References 104 publications

Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

A lucid review of Helicobacter pylori‐induced DNA damage in gastric cancer

The toxic effects of Helicobacter pylori and benzo(a)pyrene in inducing atrophic gastritis and gut microbiota dysbiosis in Mongolian gerbils

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