IBD Virome
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1464220.fastq.gz | Fastqsanger.gz | |||
| ERR1464230.fastq.gz | Fastqsanger.gz | |||
| ERR1464240.fastq.gz | Fastqsanger.gz | |||
| ERR1464250.fastq.gz | Fastqsanger.gz | |||
| ERR1464260.fastq.gz | Fastqsanger.gz |
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Project description:Purpose The role of intestinal flora in carcinogenesis and chemotherapy efficacy has been increasingly studied; however, comparisons between oral and intestinal flora remain limited. This study aimed to identify the microbial changes in urothelial carcinoma (UC) by analyzing oral saliva and stool samples from healthy individuals and patients. We also examined the association between microbial composition and immune checkpoint inhibitor (ICI) response. Methods A total of 20 healthy individuals and 38 patients with UC were analyzed. Among them, 27 patients with UC underwent ICI treatment. Oral saliva and stool samples were analyzed for 16S rRNA sequences to assess bacterial composition. Operational taxonomic units were generated, and phylogenetic analysis was performed using the 16S Metagenomics app whithin the Illumina BaseSpace Sequence Hub. Results Patients with UC showed higher Veillonellaceae and Prevotellaceae levels in saliva and stool, with lower levels of these bacteria associated with more prolonged overall survival and progression-free survival, particularly Veillonellaceae in stool. A higher neutrophil-to-lymphocyte ratio correlated with increased levels of these bacteria. Conclusion Veillonellaceae and Prevotellaceae are potential microbial biomarkers of survival outcomes and ICI efficacy in patients with UC. Non-invasive oral microbial sampling may facilitate personalized cancer treatment strategies.
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Project description:Background and aims: Gene mutations or variants leading to insufficient reactive oxygen species (ROS) production have been associated with inflammatory bowel disease (IBD). In particular, 40-50% of patients with chronic granulomatous disease have IBD (CGD-IBD). CGD is caused by inherited defects in any one of the 5 subunits forming the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex 2 (NOX2), leading to severely reduced or absent phagocyte-derived ROS production. While conventional IBD therapies can treat CGD-IBD, their benefits must be weighed against the risk of infection in this immune compromised population. Understanding the impact of NOX2 defects on the composition and function of the intestinal microbiota may lead to the identification of treatments for CGD-IBD. Methods: We evaluated GI symptom and quality of life scores, and clinical biomarkers of local (i.e. fecal occult blood and calprotectin) and systemic (i.e. CBC, CRP, ESR, and albumin) inflammation in a cohort of 79 patients with CGD, 8 mutation carriers and 17 healthy controls followed at the National Institutes of Health (NIH). We profiled the intestinal microbiome by 16S rRNA (V4 region) sequencing and the stool metabolome by mass spectrometry in all fecal samples, and further validated our findings by profiling the stool microbiome in a second cohort of 36 patients with CGD recruited from 11 centers across North-America through the Primary Immune Deficiency Treatment Consortium (PIDTC). Predictive functional profiling of the microbial communities based on 16S rRNA sequencing was also performed. Results: After controlling for significant variables, we show decreased alpha diversity and identified distinct intestinal microbiome and metabolomic profiles in patients with CGD compared to healthy individuals. In particular, we observed enrichment for Erysipelatoclostridium spp., Sellimonas spp. and Lachnoclostridium spp. in stool samples from patients with CGD. Despite differences in alpha and beta diversity in samples from the NIH compared to the PIDTC cohort, there were several bacterial taxa that correlated significantly between both cohorts. We further demonstrate that patients with active IBD and/or a history of IBD have a distinct microbiome and metabolomic profile compared to patients without CGD-IBD and identified bacterial taxa to be evaluated as potential markers of disease severity, as well as targets for future therapeutic interventions. Conclusions: Intestinal microbiome and metabolomic signatures distinguished patients with CGD and CGD-IBD and identified microbial and metabolomic candidates to be further evaluated as potential targets to improve the management of patients with CGD-IBD.
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