Generated on: 06-21-24 01:19:13

Studies Unique Samples per Visibility Status Public Samples per Data Type Users Jobs
public: 787
private: 175
sandbox: 2,573
submitted to EBI: 849
public: 394,617
private: 116,373
sandbox: 547,413
submitted to EBI: 315,251
submitted to EBI (prep): 371,707
16S: 363,648
18S: 12,040
ITS: 14,649
Metagenomic: 64,919
Full Length Operon: 803
Metatranscriptomic: 11,797
Metabolomic: 407
Genome Isolate: 1,131
13,187 768,806

Check out this random public study from the database!

To investigate whether three stimuli which result in hypochlorhydria, namely H. pylori-induced atrophic gastritis, autoimmune atrophic gastritis and proton pump inhibitor use cause specific changes to the composition of the gastric microbiota. In addition, to determine if the gastric microbiota that is present in these conditions contributes towards the specific gastric tumour risk that is associated with each of these hypochlorhydric states

Several conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Helicobacter pylori-induced atrophic gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk. 95 patients (in groups representing normal stomach, PPI treated, H. pylori gastritis, H. pylori-induced atrophic gastritis and autoimmune atrophic gastritis) were selected from a cohort of 1400. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq). Samples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. Patients with autoimmune atrophic gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. H. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. H. pylori-induced atrophic gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. Pathway analysis suggested that glucose-6-phospahte1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic gastritis versus autoimmune atrophic gastritis, and that both these groups showed increases in fumarate reductase. Conclusion: Autoimmune and H. pylori-induced atrophic gastritis were associated with different gastric microbial profiles. PPI treated patients showed relatively few alterations in the gastric microbiome compared to healthy subjects.

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