2022
DOI: 10.1155/2022/2944156
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Immunological Perspective: Helicobacter pylori Infection and Gastritis

Abstract: Helicobacter pylori is a spiral-shaped gram-negative bacterium. Its infection is mainly transmitted via oral-oral and fecal-oral routes usually during early childhood. It can achieve persistent colonization by manipulating the host immune responses, which also causes mucosal damage and inflammation. H. pylori gastritis is an infectious disease and results in chronic gastritis of different severity in near all patients with infection. It may develop from acute/chronic inflammation, chronic atrophic gastritis, i… Show more

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Cited by 36 publications
(49 citation statements)
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References 197 publications
(215 reference statements)
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“…H. pylori persistent colonization causes the dysbiosis of gut microbiota, maybe via the alterations of microenvironment, host immunity and cytokines, and modulating metabolic hormones, which may further contribute to AIDs 157,158 . H. pylori infection activates a comprehensive host immune responses and a dynamically balanced pro‐ and anti‐inflammatory cytokines network, which may also be involved in AIGs pathogenesis 107 . For example, pathogenic function of Th17 cells, 159 regulatory T cells, 160 natural killer T cells, 161 and neutrophils 162 have been implicated in the pathogenesis of many AIDs, which means the unbalance between host immune activation and inhibition to further cause the damage and inflammation of the body's own cells.…”
Section: Is the Characteristic Associated With Extra‐gastric Diseases...mentioning
confidence: 99%
See 1 more Smart Citation
“…H. pylori persistent colonization causes the dysbiosis of gut microbiota, maybe via the alterations of microenvironment, host immunity and cytokines, and modulating metabolic hormones, which may further contribute to AIDs 157,158 . H. pylori infection activates a comprehensive host immune responses and a dynamically balanced pro‐ and anti‐inflammatory cytokines network, which may also be involved in AIGs pathogenesis 107 . For example, pathogenic function of Th17 cells, 159 regulatory T cells, 160 natural killer T cells, 161 and neutrophils 162 have been implicated in the pathogenesis of many AIDs, which means the unbalance between host immune activation and inhibition to further cause the damage and inflammation of the body's own cells.…”
Section: Is the Characteristic Associated With Extra‐gastric Diseases...mentioning
confidence: 99%
“…We believe that, on one hand, both these two diseases and H. pylori infection are related to eating habits, which may be a confounding factor. On the other hand, H. pylori infection can induce chronic and systematic inflammation, 107,108 which may be a pathogenic factor. And possible association between H. pylori infection and hepatobiliary diseases, ophthalmic diseases, dermatologic diseases, and chronic kidney diseases also require further research to establish cause-effect relationship and a well-defined pathogenic pathway, which means that H. pylori eradication will have therapeutic effects.…”
Section: Is the Char Ac Teris Ti C A Sso Ciated With E X Tr A-g A S T...mentioning
confidence: 99%
“…In addition, all the precancerous conditions of GC including chronic atrophic gastritis (CAG), metaplasia, foveolar hyperplasia, and gastric hyperplastic polyps derived from the gastric epithelium are commonly caused by H. pylori infection [ 6 ]. Immunologically, it can evade host immune clearance and persistently colonize the niches, ultimately leading to the activation of pattern recognition receptors on antigen-presenting cells, gastric epithelial cells, and neutrophils [ 7 ]. In addition, H. pylori induces the activation of NF- κ B of gastric epithelial cells and leukocytes [ 7 ], contributing to the long-term colonization of H. pylori , chronic inflammatory microenvironment, and abnormal apoptosis, which further leads to accumulating mutations and malignant transformation of gastric epithelial cells [ 8 , 9 ].…”
Section: Introductionmentioning
confidence: 99%
“…Immunologically, it can evade host immune clearance and persistently colonize the niches, ultimately leading to the activation of pattern recognition receptors on antigen-presenting cells, gastric epithelial cells, and neutrophils [ 7 ]. In addition, H. pylori induces the activation of NF- κ B of gastric epithelial cells and leukocytes [ 7 ], contributing to the long-term colonization of H. pylori , chronic inflammatory microenvironment, and abnormal apoptosis, which further leads to accumulating mutations and malignant transformation of gastric epithelial cells [ 8 , 9 ]. However, senescence associated with aging and chronic inflammation may contribute to the neoplastic transformation [ 9 , 10 ].…”
Section: Introductionmentioning
confidence: 99%
“…Considering that H. pylori is the major cause of gastric carcinoma, the World Health Organization classifies H. pylori as a class I carcinogen[ 7 , 8 ]. The discovery of H. pylori led to increased research to uncover the etiology, natural history, and prognosis of HAG[ 9 , 10 ]. The Kyoto Global Consensus Report on HAG recommended that all individuals with H. pylori infection should receive eradication therapy to prevent gastric cancer[ 1 ].…”
Section: Introductionmentioning
confidence: 99%