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Complex genome-microbiome link may influence risk for IBD
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New research data suggest that complex interactions between the genetics of people and their gut microbiota may influence their risk for inflammatory bowel disease.
“The intestinal bacteria, or ‘gut microbiome,’ you develop at a very young age can have a big impact on your health for the rest of your life,” Dan Knights, PhD, assistant professor in the department of computer science and engineering and the Biotechnology Institute at the University of Minnesota, said in a press release. “We have found groups of genes that may play a role in shaping the development of imbalanced gut microbes.”
Knight and colleagues tested known IBD-associated genetic loci for links to taxonomic composition of gut microbiota in three independent cohorts that included 474 adults with IBD (aged 18-75 years) from the United States, Canada and the Netherlands. They collected 16S ribosomal RNA gene sequences from intestinal biopsies and host genotype using the Immunochip platform. They then tested for correlations between relative abundance of bacterial taxa and the number of minor alleles at 163 genetic loci known to be associated with IBD risk, specifically targeting the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) gene exon.
Across two cohorts, they found that there was a significant association between NOD2 risk allele count and increased relative abundance of Enterobacteriaceae, with a similar trend observed in the third cohort. Microbiota associations with significance validated by a false discovery rate of less than 0.25 also were detected for 48 other host genes. They also found that antibiotics are an additional risk factor for IBD-related microbial dysbiosis.
“Although our data are cross-sectional and therefore cannot define causality, our analyses demonstrate complex host genetic associations with taxonomic and metabolic dysbiosis in humans,” the researchers wrote. “These include implications of microbiome-wide associations with TNFSF15, IL12B, and with innate immune response, inflammatory response, and the JAK-STAT pathway, as well as NOD2-related increases in Enterobacteriaceae relative abundance.”
“In many cases, we’re still learning how these bacteria influence our risk of disease, but understanding the human genetics component is a necessary step in unraveling the mystery,” Knights said.
Disclosure: The researchers report no relevant financial disclosures.
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