Old and New Aspects of <i>H. pylori</i>-Associated Inflammation and Gastric Cancer
<i>H. pylori</i> 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 t...
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| Main Authors: | , , |
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| Format: | Book |
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MDPI AG,
2022-07-01T00:00:00Z.
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| Summary: | <i>H. pylori</i> 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 <i>H. pylori</i> infection. Although, this cytokine was initially identified to exert a chemoattracting effect that represents a trigger for the activation of inflammatory cells within <i>H.</i>-<i>pylori</i>-infected mucosa, more recent studies failed in encountering any association between IL-8 and <i>H. pylori</i> 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 <i>H.</i>-<i>pylori</i>-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 <i>H. pylori</i> infection. IL-10 downregulates both cytotoxic inflammatory responses and cell-mediated immune responses. <i>H. pylori</i> 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 <i>H. pylori</i> to the host's cells and their subsequent colonization. The role of <i>H.</i>-<i>pylori</i>-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 <i>H.</i>-<i>pylori</i>-associated gastric cancer. |
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| Item Description: | 10.3390/children9071083 2227-9067 |