2019
DOI: 10.3748/wjg.v25.i37.5578
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Abstract: Helicobacter pylori (H. pylori) is a gram-negative bacterium that infects approximately 4.4 billion individuals worldwide. However, its prevalence varies among different geographic areas, and is influenced by several factors. The infection can be acquired by means of oral-oral or fecal-oral transmission, and the pathogen possesses various mechanisms that improve its capacity of mobility, adherence and manipulation of the gastric microenvironment, making possible the colonization of an organ with a highly acidi… Show more

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Cited by 168 publications
(145 citation statements)
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References 116 publications
(111 reference statements)
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“…As one of the most common pathogenic bacteria in the digestive system, H. pylori infections have been shown to be closely related with the development of chronic gastritis, gastric ulcers, and gastric cancer. Various antigens and toxins produced by H. pylori can cause cellular vacuolization, mitochondrial dysfunction, and endoplasmic reticulum-mediated stress, all of which lead to the generation of oxidative stress, which is recognized by the immune system and activates the transcriptional upregulation of pro-inflammatory cytokines and chemokines triggering a series of inflammatory responses (16,17). H. pylori can also activate the immune system via the brain-gut axis and via the regulation of gastrointestinal hormones, resulting in increased secretion of gastrin, cholecystokinin, and other gastrointestinal hormones, and increased activity of intestinal smooth muscle cells.…”
Section: ' Discussionmentioning
confidence: 99%
“…As one of the most common pathogenic bacteria in the digestive system, H. pylori infections have been shown to be closely related with the development of chronic gastritis, gastric ulcers, and gastric cancer. Various antigens and toxins produced by H. pylori can cause cellular vacuolization, mitochondrial dysfunction, and endoplasmic reticulum-mediated stress, all of which lead to the generation of oxidative stress, which is recognized by the immune system and activates the transcriptional upregulation of pro-inflammatory cytokines and chemokines triggering a series of inflammatory responses (16,17). H. pylori can also activate the immune system via the brain-gut axis and via the regulation of gastrointestinal hormones, resulting in increased secretion of gastrin, cholecystokinin, and other gastrointestinal hormones, and increased activity of intestinal smooth muscle cells.…”
Section: ' Discussionmentioning
confidence: 99%
“…Urease, in addition to its role in acid neutralization, contributes to H.p. pathogenicity by production ammonia (disrupts cell junctions and damages epithelium) and reactive oxygen species (ROS), activating lipoxygenase, inducing angiogenesis, hypoxia-induced factor and apoptosis [ 26 , 27 , 28 , 29 , 30 ]. The helical shape and flagella, two factors responsible for bacterial mobility, also contribute to colonization and persistence of the infection (allow H.p.…”
Section: Brief Overview Of Helicobacter Pylorimentioning
confidence: 99%
“…The most studied virulence factors implicated in the pathogenicity of H.p. are produced by strains containing the following genes [ 29 , 31 ]: cytotoxin-associated gene A (cagA), vacuolating cytotoxin gene (vacA), duodenal ulcer (DU) promoting gene (dupA), induced by contact with epithelium gene (iceA), blood group antigen-binding adhesin (babA), sialic acid binding adhesin (sabA), outer inflammatory protein A (oipA), adherence-associated lipoprotein A and B (alpA/B), H.p. outer membrane protein Q (hopQ), gamma-glutamyl transpeptidase (GGT) and high-temperature requiring protein (HtrA).…”
Section: Brief Overview Of Helicobacter Pylorimentioning
confidence: 99%
“…The major factor that affects the rates of cure from H. pylori infection is the sufficient inhibition of acid secretion using the anti-secretory agents such as proton pump inhibitors (PPIs) [5,6]. However, the incidence of H. pylori infection and its sufficient eradication using pharmacological therapies are also affected by genetic factors, such as those affecting inflammatory cytokines and variants of the genes encoding drug-metabolizing enzymes and drug transporters [1,7,8].…”
Section: Introductionmentioning
confidence: 99%