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Do microbial backups maintain butyrate-related gene expression when dominant contributors decline in Crohn’s?
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Different microbes can carry genes for the same metabolic function. Do these genetic backups become active backups when a dominant contributor declines in Crohn’s disease?
Public longitudinal IBDMDB data contain paired microbial DNA/RNA profiles and clinical metadata. For butyrate-related pathways, the question is whether declines in the DNA abundance of dominant contributors are followed by increased transcription from alternative carriers, while community-normalized pathway transcription is maintained.
Where repeated fecal calprotectin measurements permit, is failed compensation followed by increased intestinal inflammation?
Previous research has examined DNA/RNA differences and functional redundancy in Crohn’s. The proposed contribution is to distinguish compensation success from failure during within-person microbial changes, rather than simply measure how many microbes carry the same genes.
This could help explain why some microbial communities preserve function despite changes in composition. It could also identify responsive functions worth investigating in future microbiome therapies, without establishing that any probiotic or treatment works.
RNA measures gene expression, not actual butyrate production. Interpretation would depend on normalization, participant-level analysis, sampling intervals, medication and antibiotic records, and enough usable contributor-decline events. Observational associations would not establish causation.
Data: https://ibdmdb.org/results
Related DNA/RNA study: https://pubmed.ncbi.nlm.nih.gov/29311644/
Related Crohn’s redundancy study: https://doi.org/10.1186/s40168-019-0631-8
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