&lt;p&gt;The Influence of &lt;em&gt;IL-1B&lt;/em&gt; Gene Polymorphisms on &lt;em&gt;H. pylori&lt;/em&gt; Infection and Triple Treatment Response Among Jordanian Population&lt;/p&gt;

Shakhatreh, Muhamad Ali K.; Khabour, Omar F.; Alzoubi, Karem H.; Hani, Mohammad Bani; Abu-Siniyeh, Ahmed; Bashir, Nabil; Sabi, Salsabeel H; Mahafdah, Mahmoud

doi:10.2147/tacg.s253778

Cited by 7 publications

(7 citation statements)

References 54 publications

(63 reference statements)

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“…Shakhatreh, et al conducted a study on the Jordanian population to determine the association between IL-1 gene polymorphism and H. pylori infection. -31T/C polymorphism was found significantly associated with H. pylori infection, particularly the TT genotype [22]. Those statements are reinforced by a meta-analysis by Ma et al They focused on polymorphism in genes that code IL-1.…”

Section: Mechanism Of Immune Evasion Of H Pylorimentioning

confidence: 97%

Immunology of Helicobacter pylori Infection

Darmadi¹,

Ruslie²

2022

Immunology of the GI Tract - Recent Advances

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Helicobacter pylori (H. pylori) is the most common infecting microorganism in humans. H. pylori had coexisted with humans for 30,000 years ago and developed extensive survival adaptations. The infection is both active and chronic and leads to several disorders from chronic gastritis to gastric adenocarcinoma. The prevalence of H. pylori infection is still high in developing countries. The burden of disease due to infection is also heavy. The persistence of infection is the basis of diseases. H. infection activates innate and adaptive immune responses but the immune response fails to eradicate the infection. H. pylori is able to evade both innate and adaptive immune responses. It can neutralize gastric acid, elicit autoimmunity toward parietal cells, prevent phagocytosis, induce apoptosis of immune cells, inhibit lymphocyte proliferation, disrupt imbalance between humoral and cellular adaptive immune responses, promote regulatory T cell activity, and trigger genetic rearrangement. Host factor is involved in the incidence of H. pylori infection and its complications. Reinfection after eradication is common. Multiple drug resistance has also emerged. Vaccination is a promising management approach to eradicate H. pylori and prevent diseases it caused. The development of the vaccine itself needs to consider the immune escape mechanism of H. pylori.

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Section: Mechanism Of Immune Evasion Of H Pylorimentioning

confidence: 97%

Immunology of Helicobacter pylori Infection

Darmadi¹,

Ruslie²

2022

Immunology of the GI Tract - Recent Advances

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“…In addition, genetic variants in the promoter regions of the IL-1β gene were recently shown to alter cytokine expression, creating a hypoacidity environment involved in enabling the long-term persistence and colonization of H. pylori [ 82 ]. Nevertheless, the influence of IL-1β gene polymorphisms on H. pylori infection might be closely related to ethnicity or geographical area [ 83 ]. The genetic variants of this cytokine seem to also influence the success of H. pylori eradication regimens in patients with functional dyspepsia [ 84 ].…”

Section: The Trialogue Between H Pylori Cytokines...mentioning

confidence: 99%

“…IL-1β gene polymorphisms influence H. pylori infection and might be closely related to ethnicity or geographical area [ 83 ]…”

Section: The Trialogue Between H Pylori Cytokines...mentioning

confidence: 99%

Old and New Aspects of H. pylori-Associated Inflammation and Gastric Cancer

Meliţ

Mărginean

2022

Children

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H. pylori is involved in the development of 80% of gastric cancers and 5.5% of all malignant conditions worldwide. Its persistence within the host’s stomach causes chronic inflammation, which is a well-known hallmark of carcinogenesis. A wide range of cytokines was reported to be involved in the initiation and long-term persistence of this local and systemic inflammation. IL-8 was among the first cytokines described to be increased in patients with H. pylori infection. Although, this cytokine was initially identified to exert a chemoattracting effect that represents a trigger for the activation of inflammatory cells within H.-pylori-infected mucosa, more recent studies failed in encountering any association between IL-8 and H. pylori infection. IL-6 is a multifunctional, pleiotropic and multipotent cytokine involved in mediating the interaction between innate and adaptive immunity with a dichotomous role acting as both a proinflammatory and an anti-inflammatory cytokine depending on the signaling pathway. IL-1α functions as a promoter of angiogenesis and vascular endothelial cell proliferation in gastric carcinoma since it is closely related to H.-pylori-induced inflammation in children. IL-1β is an essential trigger and enhancer of inflammation. The association between a low IL-1β level and an increased TNF-α level might be considered a risk factor for peptic ulcer disease in the setting of H. pylori infection. IL-10 downregulates both cytotoxic inflammatory responses and cell-mediated immune responses. H. pylori uses the immunosuppressive role of IL-10 to favor its escape from the host’s immune system. TGFβ is a continuous inflammatory mediator that promotes the adherence of H. pylori to the host’s cells and their subsequent colonization. The role of H.-pylori-induced inflammatory responses in the onset of gastric carcinogenesis seems to represent the missing puzzle piece for designing effective preventive and therapeutic strategies in patients with H.-pylori-associated gastric cancer.

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“…In addition, genetic variants in the promoter regions of the IL-1β gene were recently shown to alter cytokine expression, creating a hypoacidity environment involved in enabling the longterm persistence and colonization of H. pylori [82]. Nevertheless, the influence of IL-1β gene polymorphisms on H. pylori infection might be closely related to ethnicity or geographical area [83]. The genetic variants of this cytokine seem to also influence the success of H. pylori eradication regimens in patients with functional dyspepsia [84].…”

Section: Il-1βmentioning

confidence: 99%

Old and New Aspects of H. pylori-Associated Inflammation and Gastric Cancer

Dinca,

Meliț,

Marginean

2022

Prime Archives in Medicine

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H. pylori is involved in the development of 80% of gastric cancers and 5.5% of all malignant conditions worldwide. Its persistence within the host's stomach causes chronic inflammation, which is a well-known hallmark of carcinogenesis. A wide range of cytokines was reported to be involved in the initiation and long-term persistence of this local and systemic inflammation. IL-8 was among the first cytokines described to be increased in patients with H. pylori infection. Although, this cytokine was initially identified to exert a chemoattracting effect that represents a trigger for the activation of inflammatory cells within H.-pylori-infected mucosa, more recent studies failed in encountering any association between IL-8 and H. pylori infection. IL-6 is a multifunctional, pleiotropic and multipotent cytokine involved in mediating the interaction between innate and adaptive immunity with a dichotomous role acting as both a proinflammatory and an antiinflammatory cytokine depending on the signaling pathway. IL-1α functions as a promoter of angiogenesis and vascular endothelial cell proliferation in gastric carcinoma since it is closely related to H.-pylori-induced inflammation in children. IL-1β is an essential trigger and enhancer of inflammation. The association between a low IL-1β level and an increased TNF-α level might be considered a risk factor for peptic ulcer disease in the setting of H. pylori infection. IL-10 downregulates both cytotoxic inflammatory responses and cell-mediated immune responses. H. pylori uses the immunosuppressive role of IL-10 to favor its escape from the host's immune system. TGFβ is a continuous inflammatory mediator that promotes the adherence of H. pylori to the host's cells and their subsequent colonization. The role of H.-pyloriwww.videleaf.com induced inflammatory responses in the onset of gastric carcinogenesis seems to represent the missing puzzle piece for designing effective preventive and therapeutic strategies in patients with H.-pylori-associated gastric cancer.

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<p>The Influence of <em>IL-1B</em> Gene Polymorphisms on <em>H. pylori</em> Infection and Triple Treatment Response Among Jordanian Population</p>

Cited by 7 publications

References 54 publications

Immunology of Helicobacter pylori Infection

Immunology of Helicobacter pylori Infection

Old and New Aspects of H. pylori-Associated Inflammation and Gastric Cancer

Old and New Aspects of H. pylori-Associated Inflammation and Gastric Cancer

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