scholarly journals Host Wnt/β-catenin pathway triggered by Helicobacter pylori correlates with regression of gastric intestinal metaplasia after H. pylori eradication

2009 ◽  
Vol 58 (5) ◽  
pp. 567-576 ◽  
Author(s):  
Kuei-Hsiang Hung ◽  
Jiunn-Jong Wu ◽  
Hsiao-Bai Yang ◽  
Li-Ju Su ◽  
Bor-Shyang Sheu
Keyword(s):  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
Glycogen Synthase ◽  
Nucleotide Polymorphisms ◽  
Ags Cells ◽  
Gastric Intestinal Metaplasia ◽  
Before And After ◽  
Cox 2 ◽  
H Pylori ◽  
High Level

Helicobacter pylori eradication can reverse gastric intestinal metaplasia (IM) in some but not all patients. H. pylori induces high levels of nuclear β-catenin staining in IM tissues, as well as overexpression of cyclooxygenase-2 (COX-2). This study investigated whether the Wnt/β-catenin pathway plays a role in IM regression following H. pylori eradication. Sixty-five H. pylori-infected patients with IM who had achieved successful H. pylori eradication provided paired gastric samples before and after eradication to analyse the persistence of IM, and to assess COX-2 and nuclear β-catenin expression. The host genotypes of single nucleotide polymorphisms (SNPs) of the COX-2, β-catenin (CTNNB1) and adenomatous polyposis coli (APC) genes were analysed. In addition, expression of β-catenin, E-cadherin and phosphorylated and unphosphorylated glycogen synthase kinase 3β (GSK-3β) in cell lines challenged with H. pylori isolates from patients with and without IM persistence was compared by immunoanalysis. After a mean 33.9-month follow-up after H. pylori eradication, 44 patients (67.7 %) with IM persistence had a higher rate of high-level nuclear β-catenin expression in IM tissue than those without IM persistence (P=0.008). The patients with IM persistence had a higher rate of AA, GG and AA APC SNP genotypes at positions 4479, 5268 and 5465, respectively, than the patients without IM persistence (P=0.022). The H. pylori isolates from the patients with IM regression after H. pylori eradication induced more phospho-GSK-3β in AGS cells than isolates from patients with IM persistence (P=0.011). It is likely that interactions with H. pylori and the patient's Wnt/β-catenin genetic predisposition determine the outcome of IM persistence following H. pylori eradication.

scholarly journals Gastric microbes associated with gastric inflammation, atrophy and intestinal metaplasia 1 year after Helicobacter pylori eradication

Gut ◽  
2020 ◽  
Vol 69 (9) ◽  
pp. 1572-1580 ◽  
Author(s):  
Joseph J Y Sung ◽  
Olabisi Oluwabukola Coker ◽  
Eagle Chu ◽  
Chun Ho Szeto ◽  
Simson Tsz Yat Luk ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
Inositol Phosphate ◽  
Eradication Therapy ◽  
Treated Group ◽  
Oral Bacteria ◽  
Microbial Interactions ◽  
Bacterial Taxonomy ◽  
Before And After ◽  
H Pylori

ObjectiveHelicobacter pylori is associated with gastric inflammation, precancerous gastric atrophy (GA) and intestinal metaplasia (IM). We aimed to identify microbes that are associated with progressive inflammation, GA and IM 1 year after H. pylori eradication.DesignA total of 587 H. pylori–positive patients were randomised to receive H. pylori eradication therapy (295 patients) or placebo (292 patients). Bacterial taxonomy was analysed on 404 gastric biopsy samples comprising 102 pairs before and after 1 year H. pylori eradication and 100 pairs before and after 1 year placebo by 16S rRNA sequencing.ResultsAnalysis of microbial sequences confirmed the eradication of H. pylori in treated group after 1 year. Principal component analysis revealed distinct microbial clusters reflected by increase in bacterial diversity (p<0.00001) after H. pylori eradication. While microbial interactions remained largely unchanged after placebo treatment, microbial co-occurrence was less in treated group. Acinetobacter lwoffii, Streptococcus anginosus and Ralstonia were enriched while Roseburia and Sphingomonas were depleted in patients with persistent inflammation 1 year after H. pylori eradication. A distinct cluster of oral bacteria comprising Peptostreptococcus, Streptococcus, Parvimonas, Prevotella, Rothia and Granulicatella were associated with emergence and persistence of GA and IM. Probiotic Faecalibacterium praustznii was depleted in subjects who developed GA following H. pylori eradication. Functional pathways including amino acid metabolism and inositol phosphate metabolism were enriched while folate biosynthesis and NOD-like receptor signalling decreased in atrophy/IM-associated gastric microbiota.ConclusionThis study identified that gastric microbes contribute to the progression of gastric carcinogenesis after H. pylori eradication.

scholarly journals Acquisition of double mutation in gyrA caused high resistance to sitafloxacin in Helicobacter pylori after unsuccessful eradication with sitafloxacin-containing regimens

2017 ◽  
Vol 6 (3) ◽  
pp. 391-397 ◽  
Author(s):  
Hideki Mori ◽  
Hidekazu Suzuki ◽  
Juntaro Matsuzaki ◽  
Tatsuhiro Masaoka ◽  
Takanori Kanai
Keyword(s):  
Helicobacter Pylori ◽  
Randomized Study ◽  
University Hospital ◽  
Fluoroquinolone Resistance ◽  
Infection Prevalence ◽  
Double Mutation ◽  
Before And After ◽  
Pre Treatment ◽  
H Pylori ◽  
High Level

Background and aim Although sitafloxacin (STFX)-containing regimens are effective rescue treatments for Helicobacter pylori infection, prevalence of fluoroquinolone resistance in H. pylori has increased rapidly worldwide. The change in resistance levels and gyrA mutations, a major cause of fluoroquinolone resistance, after unsuccessful STFX-containing treatment has not been investigated. Methods We conducted a retrospective, non-randomized study to compare the minimum inhibitory concentrations (MICs) of STFX and the location of gyrA mutations in H. pylori before and after unsuccessful eradication with STFX-containing regimens at Keio University Hospital between December 2011 and March 2015. Results A total of 266 patients treated with STFX-containing regimens for third-line H. pylori eradication were evaluated. Double mutations in gyrA were acquired by 20.8% of strains that exhibited seven-fold increased STFX MICs, compared to pre-treatment MICs. The STFX MICs did not increase, however, when the location of the gyrA mutations did not change after treatment. Double mutations in gyrA developed in 60.0% of the strains in which eradication failed, which exhibited a baseline mutation at position D91, and in 11.1% of strains with baseline mutations at position N87. Conclusion Acquisition of double mutations in gyrA evoked high-level resistance to STFX in H. pylori after unsuccessful eradication with STFX-containing regimens.

scholarly journals Antacids may increase the appearance of white opaque substance in Helicobacter pylori-eradicated gastric epithelial neoplasia

2019 ◽  
Vol 07 (09) ◽  
pp. E1144-E1149 ◽  
Author(s):  
Kurato Wada ◽  
Tetsuya Ueo ◽  
Hirotoshi Yonemasu ◽  
Kazumi Togo ◽  
Shotaro Inoue ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Juice ◽  
Narrow Band ◽  
Narrow Band Imaging ◽  
Helicobacter Pylori Eradication ◽  
Gastric Intestinal Metaplasia ◽  
Gastric Epithelial Neoplasia ◽  
Acid Recovery ◽  
Before And After ◽  
H Pylori

Abstract Background and study aims White opaque substance (WOS) in gastric epithelial neoplasia is helpful for qualitative diagnosis of neoplasia. We hypothesized that WOS of neoplasia is strongly influenced by acid recovery after Helicobacter pylori eradication, similar to that of gastric intestinal metaplasia. The aim of this study was to investigate whether antacids increase the appearance of the WOS in H. pylori-eradicated neoplasia. Patients and methods A total of 38 gastric epithelial neoplasias (12 adenomas and 26 adenocarcinomas) detected after H. pylori eradication were retrospectively evaluated. Presence or absence of WOS was evaluated by magnifying endoscopy with narrow band imaging before and after antacid administration. The pH of collected gastric juice was also measured. Study endpoints were (1) prevalence of WOS in the neoplasia before and after antacid administration, and the histological difference (adenoma and adenocarcinoma); and (2) relationship between the prevalence of WOS and gastric juice pH. Results WOS prevalence increased from 0 % (0/38) to 44.8% (17/38) after antacid administration. WOS prevalence in adenomas was more significantly increased compared to that in adenocarcinomas (83.3 % vs 26.9 %, P = 0.0077). Prevalence of WOS in gastric neoplasias was only observed at neutral levels of gastric juice pH, and WOS was not observed at strong acidic levels. Conclusions Antacid administration may increase the appearance of WOS in gastric epithelial neoplasia (especially adenomas) detected after H. pylori eradication with acid recovery.

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