2023
DOI: 10.1016/j.ram.2022.04.003
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Helicobacter pylori infection: A balance between bacteria and host

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Cited by 5 publications
(6 citation statements)
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“…48 The cytotoxin-associated gene product (CagA), the vacuolating toxin (VacA), and the adhesion protein BabA2 are three of the major virulent factors of H. pylori. [49][50][51] Studies from Brazil, Saudi, Mexico, Japan, and Laos showed that the three virulent factors might be meaningful markers of the toxicity of H. pylori and clinical outcome of patients. [52][53][54][55][56] Combination detection of serum pepsinogen I, pepsinogen II, gastrin-17, and H. pylori virulent factors might improve the precise prediction of high-risk subpopulation of gastric cancer.…”
Section: Discussionmentioning
confidence: 99%
“…48 The cytotoxin-associated gene product (CagA), the vacuolating toxin (VacA), and the adhesion protein BabA2 are three of the major virulent factors of H. pylori. [49][50][51] Studies from Brazil, Saudi, Mexico, Japan, and Laos showed that the three virulent factors might be meaningful markers of the toxicity of H. pylori and clinical outcome of patients. [52][53][54][55][56] Combination detection of serum pepsinogen I, pepsinogen II, gastrin-17, and H. pylori virulent factors might improve the precise prediction of high-risk subpopulation of gastric cancer.…”
Section: Discussionmentioning
confidence: 99%
“…Similarly, OMVs can also be released by harmful bacteria, such as the Gram-negative proteobacterium Helicobacter pylorus (Hp), whose chronic infection leads to chronic inflammation and the development of gastric cancer [ 152 , 153 ]. Hp OMVs have been shown to carry virulence genes (CagA and VacA) of the parent bacteria, which can induce the production of immunomodulatory cytokines in host macrophages and gastric epithelial cells [ 154 , 155 ]. As seen from in vitro and in vivo studies, Cy7 labeled Hp OMVs were able to infiltrate the gastric epithelium and still be detectable even 24 h after injection, causing inflammation and contributing to the development of gastric cancer [ 156 ].…”
Section: Biology Of Extracellular Vesiclesmentioning
confidence: 99%
“…As previously noted, the majority of patients infected with H. pylori exhibit histologic gastritis, and the phenotype of this gastritis will influence the progression of symptoms [48][49][50]. Most of the patients have a mild gastritis phenotype that in general is asymptomatic and do not affect the acid secretion, 10 to 15% presents the duodenal ulcer phenotype that affects the secretory function with a higher production of gastrin and acid secretion, with disturbances in the inhibitory control of acid secretion leading to dyspeptic symptoms and/or duodenal ulcer, and less than 1% present the gastric cancer phenotype that culminates in a strong reduction or absence of acid secretion, leading to severe atrophic gastritis, intestinal metaplasia and gastric cancer [21,34,[51][52][53]. In Figure 2 the treatment and strain genetic mutations have been determined and described in literature [58,59].…”
Section: Introductionmentioning
confidence: 99%