PTH-100 The effect of gastric helicobacter pylori infection on the intestinal microbiome of ibd patients

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Abstract

Introduction

Helicobacter pylori is a Gram-negative bacterium, which infects over 50% of the population worldwide. However, only a subset of these infections result in gastrointestinal diseases, such as peptic ulceration (10%) and gastric cancer (2%). Several epidemiological studies have revealed that people who carry H. pylori are at a decreased risk of developing IBD. However, a mechanistic understanding of the association between H. pylori infection and IBD is still unknown. Unlike any other microbial species, once H. pylori colonises its gastric niche, it is able to dominate the gastric microbiome, representing 90%–95% of the total microbial population. Therefore, we hypothesised that the presence of H. pylori in the upper gastrointestinal (GI) tract prevents the colonisation of the lower GI tract with microbial species associated with the pathogenesis of IBD.

Method

To test this, we collected stool samples from IBD patients (comprising Ulcerative Colitis and Crohn’s disease patients) and determined their H. pylori status using a stool antigen test. We then characterised the intestinal microbiota of H. pylori positive (n=9) and negative IBD patients (n=18), by amplifying the V4 hyper-variable region of the 16S rRNA gene from faecal DNA. To determine the predominant phyla, these products were sequenced using the Illumina MiSeq and data analysis was performed using the QIIME pipeline and GreenGenes database.

Results

Interestingly, bacterial community structure revealed that there is a strong trend towards a decrease of Proteobacteria and an increase of Bacteroidetes in H. pylori positive IBD patients. Of note, IBD is generally characterised by an increase in Proteobacteria and a decrease in Bacteroidetes. Furthermore, using PICRUSt to investigate the functional composition of the metagenomes, we found that the H. pylori positive IBD patients displayed significant functional differences, including decreased bacterial motility and chemotaxis (p=<0.05), demonstrating suppression of virulence traits.

Conclusion

Our preliminary data suggests that the presence of H. pylori infection may promote a less pathogenic intestinal microbiome in patients with established IBD. This data provides the rationale to extend our studies with increased patient numbers and healthy controls to determine the mechanistic basis for the negative association of H. pylori infection and IBD.

Disclosure of Interest

None Declared

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