scholarly journals Transient and Persistent Gastric Microbiome: Adherence of Bacteria in Gastric Cancer and Dyspeptic Patient Biopsies after Washing

2020 ◽  
Vol 9 (6) ◽  
pp. 1882 ◽  
Author(s):  
Malene R. Spiegelhauer ◽  
Juozas Kupcinskas ◽  
Thor B. Johannesen ◽  
Mindaugas Urba ◽  
Jurgita Skieceviciene ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Bacterial Diversity ◽  
Large Scale ◽  
Amplicon Sequencing ◽  
Rrna Gene ◽  
Peptic Ulcers ◽  
Gastric Biopsies ◽  
H Pylori ◽  
Gastric Microbiota

Helicobacter pylori is a common colonizer of the human stomach, and long-term colonization has been related to development of atrophic gastritis, peptic ulcers and gastric cancer. The increased gastric pH caused by H. pylori colonization, treatment with antibiotics or proton pump inhibitors (PPI) may allow growth of other bacteria. Previous studies have detected non-Helicobacter bacteria in stomach biopsies, but no conclusion has been made of whether these represent a transient contamination or a persistent microbiota. The aim of this study was to evaluate the transient and persistent bacterial communities of gastric biopsies. The washed or unwashed gastric biopsies were investigated by cultivation and microbiota analysis (16S rRNA gene-targeted amplicon sequencing) for the distribution of H. pylori and other non-Helicobacter bacteria. The number of cultured non-Helicobacter bacteria decreased in the washed biopsies, suggesting that they might be a transient contamination. No significant differences in the bacterial diversity were observed in the microbiome analysis between unwashed and washed biopsies. However, the bacterial diversity in biopsies shown H. pylori-positive and H. pylori-negative were significantly different, implying that H. pylori is the major modulator of the gastric microbiome. Further large-scale studies are required to investigate the transient and persistent gastric microbiota.

Increased Production of Matrix Metalloproteinases in Helicobacter pylori Infection that Stimulates Gastric Cancer Stem Cells

2020 ◽  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Helicobacter Pylori ◽  
Cancer Stem Cells ◽  
Histopathological Examination ◽  
Physiological Saline ◽  
Rrna Gene ◽  
Peptic Ulcers ◽  
Gastric Cancer Stem Cells ◽  
H Pylori

Background and aim: Helicobacter pylori (H. pylori) is an incriminated pathogen causing diseases in both animals and humans and considered a zoonotic pathogen. H. pylori infection is considered a cause of gastric cancer, which rests a significant health care challenge. This study analyzes the expression pattern of matrix metalloprotein 2 (MMP-2) in patients with Helicobacter pylori-associated gastritis and the effect of H. pylori on gastric cancer stem cells, as well as study the role of helicon bacteriosis in dog in transmission of H. pylori infection to human. Materials and methods: Fifty-five of each sample (gastric biopsy, blood and stool) were collected from patients suffering from dyspepsia, chronic vomiting and perforated peptic ulcers and also from apparent healthy dogs. The investigation detected H. pylori by serological and histopathological examination. Biopsies were stored in physiological saline for identification of H. pylori by conventional time PCR. MMP-2 and Gastric cancer stem cells were then identified by immunohistochemistry. Results: Serological identification for H. pylori Antigen and Antibodies revealed (63% human, 50% dogs) and (87% human, 90% dogs) respectively were positive. Genotyping of H. pylori based on 16S rRNA gene showed 54.5% of human and 35% of dogs were positive. Immunohistochemistry revealed strong expression of CD44 in H. pylori- associated gastric cancer cases, MMP-2 expression was observed in all neoplastic lesions associated with H. pylori infection. Conclusion: H. pylori infection affects gastric mucosa and induces changes in gastric stem cells altering their differentiation and increased expression of MMP’s and CD44with a resultant potentiation of oncogenic alteration. In addition the up-regulation of both markers could be an instrumental to interpret the origination of gastric cancer.

Su1902 Molecular Analysis of Human Gastric Microbiota by Pyrosequencing for 16s rRNA Gene in Patients With Gastric Cancer Depending on H. pylori Positivity

2013 ◽  
Vol 144 (5) ◽  
pp. S-505 ◽  
Author(s):  
Nayoung Kim ◽  
Yoon Jin Choi ◽  
Ji Yeon Kim ◽  
Ryoung Hee Nam ◽  
Mi Ji Choi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
16S Rrna ◽  
16S Rrna Gene ◽  
Molecular Analysis ◽  
Rrna Gene ◽  
H Pylori ◽  
Gastric Microbiota

scholarly journals Gastric Microbiota in Helicobacter pylori-Negative and -Positive Gastritis Among High Incidence of Gastric Cancer Area

Cancers ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 504 ◽  
Author(s):  
Boldbaatar Gantuya ◽  
Hashem B. El-Serag ◽  
Takashi Matsumoto ◽  
Nadim J. Ajami ◽  
Khasag Oyuntsetseg ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Bacterial Species ◽  
Rrna Gene ◽  
Linear Discriminant ◽  
Haemophilus Parainfluenzae ◽  
Increased Risk ◽  
Comparison Groups ◽  
H Pylori ◽  
Gastric Microbiota

Helicobacter pylori (H. pylori) related chronic gastritis is a well-known major etiological factor for gastric cancer development. However, H. pylori-negative gastritis (HpN) is not well described. We aimed to examine gastric mucosal microbiota in HpN compared to H. pylori-positive gastritis (HpP) and H. pylori-negative non-gastritis group (control). Here, we studied 11 subjects with HpN, 40 with HpP and 24 controls. We performed endoscopy with six gastric biopsies. Comparison groups were defined based on strict histological criteria for the disease and H. pylori diagnosis. We used 16S rRNA gene amplicon sequencing to profile the gastric microbiota according to comparison groups. These results demonstrate that the HpP group had significantly lower bacterial richness by the operational taxonomic unit (OTU) counts, and Shannon and Simpson indices as compared to HpN or controls. The linear discriminant analysis effect size analysis showed the enrichment of Firmicutes, Fusobacteria, Bacteroidetes and Actinobacteria at phylum level in the HpN group. In the age-adjusted multivariate analysis, Streptococcus sp. and Haemophilus parainfluenzae were at a significantly increased risk for HpN (odds ratio 18.9 and 12.3, respectively) based on abundance. Treponema sp. was uniquely found in HpN based on occurrence. In this paper, we conclude that Streptococcus sp., Haemophilus parainfluenzae and Treponema sp. are candidate pathogenic bacterial species for HpN. These results if confirmed may have important clinical implications.

scholarly journals Helicobacter pylori dupA and gastric acid secretion are negatively associated with gastric cancer development

2010 ◽  
Vol 59 (12) ◽  
pp. 1484-1489 ◽  
Author(s):  
Shinobu Imagawa ◽  
Masanori Ito ◽  
Masaharu Yoshihara ◽  
Hidetaka Eguchi ◽  
Shinji Tanaka ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Duodenal Ulcer ◽  
Gastric Acid ◽  
Acid Output ◽  
Rank Test ◽  
Peptic Ulcers ◽  
Log Rank Test ◽  
H Pylori

Few reports have described the cancer prevalence of peptic ulcer patients with long-term follow-up studies. We have conducted a long-term retrospective cohort study of Japanese peptic ulcer patients and evaluated the risk factors for the occurrence of gastric cancer (GCa). A total of 136 patients diagnosed with peptic ulcers from 1975 to 1983 were enrolled. These 136 cases [102 males and 34 females; 69 gastric ulcer (GU) and 67 duodenal ulcer (DU) patients at the time of enrolment; mean follow-up period of 14.4 years (range 1–30 years)] after being matched with a tumour registry database in Hiroshima prefecture were surveyed for GCa. We investigated Helicobacter pylori duodenal ulcer promoter gene A (dupA) using paraffin-embedded gastric biopsy specimens in 56 cases. Gastric acid secretion and basal acid output (BAO) in 40 cases, and maximal acid output in 68 cases, had been measured at first diagnosis of peptic ulcers. GCa was detected in 24 patients (17 with GU, 7 with DU) during the follow-up. The prevalence of GCa was significantly higher in GU patients than in DU patients (log-rank test P<0.05). dupA-positive H. pylori was detected not only in DU patients (9/20) but also in GU patients (9/36). Gastric acid output was significantly larger in quantity in patients with dupA-positive H. pylori than in those with dupA-negative H. pylori (P<0.05). The occurrence of GCa was significantly lower in patients with dupA-positive H. pylori and a high BAO level (log-rank test P<0.05). DUs, higher acid output and dupA-positive H. pylori were negatively associated with GCa.

scholarly journals Gastrointestinal Microbiota Changes in Patients With Gastric Precancerous Lesions

2021 ◽  
Vol 11 ◽  
Author(s):  
Dehua Liu ◽  
Si Chen ◽  
Yawen Gou ◽  
Wenyong Yu ◽  
Hangcheng Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Precancerous Lesions ◽  
Alpha Diversity ◽  
Intraepithelial Neoplasia ◽  
Rrna Gene ◽  
Gastrointestinal Microbiota ◽  
Microbial Composition ◽  
16S Rrna Gene Analysis ◽  
Gastric Biopsies ◽  
Gastric Microbiota

BackgroundGastric microbiota may be involved in gastric cancer. The relationship between gastrointestinal microbes and the risk of gastric cancer is unclear. This study aimed to explore the gastric and intestinal bacteria associated with gastritis and gastric precancerous lesions. We conducted a case-control study by performing 16S rRNA gene analysis of gastric biopsies, juices, and stool samples from 148 cases with gastritis or gastric precancerous lesions from Anhui and neighboring provinces, China. And we validated our findings in public datasets.ResultsAnalysis of microbial sequences revealed decreased bacterial alpha diversity in gastric bacteria during the progression of gastritis. Helicobacter pylori was the main contributor to the decreased microbial composition and diversity in the gastric mucosa and had little influence on the microbiota of gastric juice and feces. The gastric mucosal genera Gemella, Veillonella, Streptococcus, Actinobacillus, and Hemophilus had the higher degree of centrality across the progression of gastric precancerous lesions. And Acinetobacter may contribute to the occurrence of intraepithelial neoplasia. In addition, the microbial model of H. pylori-positive gastric biopsies and feces showed value in the prediction of gastric precancerous lesions.ConclusionsThis study identified associations between gastric precancerous lesions and gastric microbiota, as well as the changes in intestinal microbiota, and explored their values in the prediction of gastric precancerous lesions.

scholarly journals Association between the relative abundance of gastric microbiota and the risk of gastric cancer: a case-control study

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Madhawa Neranjan Gunathilake ◽  
Jeonghee Lee ◽  
Il Ju Choi ◽  
Young-Il Kim ◽  
Yongju Ahn ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Relative Abundance ◽  
Protective Factor ◽  
Rrna Gene ◽  
16S Rrna Gene Analysis ◽  
Logistic Regression Models ◽  
Diverse Community ◽  
H Pylori ◽  
Study Participants ◽  
Gastric Microbiota

Abstract The human gut hosts a diverse community of bacteria referred to as the gut microbiome. We investigated the association between the relative abundance of gastric microbiota and gastric cancer (GC) risk in a Korean population. The study participants included 268 GC patients and 288 controls. DNA was extracted from gastric biopsies, and 16S rRNA gene analysis was performed. Unconditional logistic regression models were used to observe the associations. Of the participants, those who had the highest level (highest tertile) of relative Helicobacter pylori and Propionibacterium acnes abundances showed a significantly higher risk for GC after adjusting for potential confounding variables (odds ratio (OR) = 1.86, 95% confidence interval (CI) = 1.17–2.97, p for trend = 0.017 and OR = 4.77, 95% CI = 2.94–7.74, p for trend <0.001, respectively). Subjects who carried Prevotella copri had a significantly higher risk of GC than noncarriers (OR = 2.54, 95% CI = 1.42–4.55, p for trend = 0.002). There was a lower risk of GC in subjects carrying Lactococcus lactis than in noncarriers (OR = 0.21, 95% CI = 0.10–0.44, p for trend <0.001). H. pylori, P. acnes and P. copri are strong risk factors, whereas L. lactis is a protective factor, for GC development in Koreans. Further microbiome studies are warranted to verify the findings of the current study.

scholarly journals Meta-Apo improves accuracy of 16S-amplicon-based prediction of microbiome function

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Gongchao Jing ◽  
Yufeng Zhang ◽  
Wenzhi Cui ◽  
Lu Liu ◽  
Jian Xu ◽  
...  
Keyword(s):  
16S Rrna ◽  
Large Scale ◽  
Low Cost ◽  
Human Microbiome ◽  
Amplicon Sequencing ◽  
Training Sample ◽  
Rrna Gene ◽  
16S Amplicon Sequencing ◽  
Cross Platform ◽  
Functional Profiles

Abstract Background Due to their much lower costs in experiment and computation than metagenomic whole-genome sequencing (WGS), 16S rRNA gene amplicons have been widely used for predicting the functional profiles of microbiome, via software tools such as PICRUSt 2. However, due to the potential PCR bias and gene profile variation among phylogenetically related genomes, functional profiles predicted from 16S amplicons may deviate from WGS-derived ones, resulting in misleading results. Results Here we present Meta-Apo, which greatly reduces or even eliminates such deviation, thus deduces much more consistent diversity patterns between the two approaches. Tests of Meta-Apo on > 5000 16S-rRNA amplicon human microbiome samples from 4 body sites showed the deviation between the two strategies is significantly reduced by using only 15 WGS-amplicon training sample pairs. Moreover, Meta-Apo enables cross-platform functional comparison between WGS and amplicon samples, thus greatly improve 16S-based microbiome diagnosis, e.g. accuracy of gingivitis diagnosis via 16S-derived functional profiles was elevated from 65 to 95% by WGS-based classification. Therefore, with the low cost of 16S-amplicon sequencing, Meta-Apo can produce a reliable, high-resolution view of microbiome function equivalent to that offered by shotgun WGS. Conclusions This suggests that large-scale, function-oriented microbiome sequencing projects can probably benefit from the lower cost of 16S-amplicon strategy, without sacrificing the precision in functional reconstruction that otherwise requires WGS. An optimized C++ implementation of Meta-Apo is available on GitHub (https://github.com/qibebt-bioinfo/meta-apo) under a GNU GPL license. It takes the functional profiles of a few paired WGS:16S-amplicon samples as training, and outputs the calibrated functional profiles for the much larger number of 16S-amplicon samples.

scholarly journals Proteomics signature of autoimmune atrophic gastritis: towards a link with gastric cancer

2021 ◽  
Author(s):  
Ombretta Repetto ◽  
Valli De Re ◽  
Paolo Giuffrida ◽  
Marco Vincenzo Lenti ◽  
Raffaella Magris ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Tricarboxylic Acid Cycle ◽  
Differential Abundance ◽  
Expression Levels ◽  
2D Dige ◽  
Gastric Corpus ◽  
Gastric Biopsies ◽  
H Pylori ◽  
Autoimmune Atrophic Gastritis

Abstract Background Autoimmune atrophic gastritis (AAG) is a chronic disease that can progress to gastric cancer (GC). To better understand AAG pathology, this proteomics study investigated gastric proteins whose expression levels are altered in this disease and also in GC. Methods Using two-dimensional difference gel electrophoresis (2D-DIGE), we compared protein maps of gastric corpus biopsies from AAG patients and controls. Differentially abundant spots (|fold change|≥ 1.5, P < 0.01) were selected and identified by LC–MS/MS. The spots were further assessed in gastric antrum biopsies from AAG patients (without and with Helicobacter pylori infection) and from GC patients and unaffected first-degree relatives of GC patients. Results 2D-DIGE identified 67 differentially abundant spots, with 28 more and 39 less abundant in AAG-corpus than controls. LC–MS/MS identified these as 53 distinct proteins. The most significant (adjusted P < 0.01) biological process associated with the less abundant proteins was “tricarboxylic acid cycle”. Of the 67 spots, 57 were similarly differentially abundant in AAG-antrum biopsies irrespective of H. pylori infection status. The differential abundance was also observed in GC biopsies for 14 of 28 more abundant and 35 of 39 less abundant spots, and in normal gastric biopsies of relatives of GC patients for 6 and 25 spots, respectively. Immunoblotting confirmed the different expression levels of two more abundant proteins (PDIA3, GSTP gene products) and four less abundant proteins (ATP5F1A, PGA3, SDHB, PGC). Conclusion This study identified a proteomics signature of AAG. Many differential proteins were shared by GC and may be involved in the progression of AAG to GC.

Frequency of rdx A Deletion Mutation Conferring Metronidazole Resistance in Helicobacter pylori

2020 ◽  
Vol 29 (3) ◽  
pp. 59-64
Author(s):  
Hanaa M. El Maghraby ◽  
Samar Mohaseb
Keyword(s):  
Helicobacter Pylori ◽  
Epigastric Pain ◽  
Deletion Mutation ◽  
Rapid Urease Test ◽  
Rrna Gene ◽  
University Hospitals ◽  
Metronidazole Resistance ◽  
Urease Test ◽  
Gastric Biopsies ◽  
H Pylori

Background: Metronidazole is one of the antimicrobial drugs that can be used in combination with other drugs for eradication of Helicobacter pylori (H. pylori).Unfortunately, metronidazole resistance in H. plori is an increasing health problem which may be attributed to inactivation of many genes as rdx A gene. Objective: To determine the frequency of rdx A deletion mutation in H. pylori detected in infected patients attending at the Gastroenterology Unit, Zagazig University Hospitals. Methodology: Two gastric biopsies were taken from each enrolled patient by endoscopy. H.pylori detection was done by rapid urease test and polymerase chain reaction (PCR) amplification of 16S rRNA gene. Deletion mutation in rdx A gene was detected by conventional PCR. Results: Out of 134 doubled gastric biopsies obtained from 134 patients, 52.2% were positive for H. pylori. Epigastric pain, vomiting and gastritis were significantly associated with detection of H. pylori infection (p˂ 0.05). Deletion mutation of rdx A gene was detected in 28.6% of H. pylori positive specimens obtained from infected patients. Conclusion: Deletion mutation of rdx A gene is a frequent determinant of rdx A inactivation conferring metronidazole resistance among H. pylori.

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