PUBLICATION
Disturbances in Microbial and Metabolic Communication across the Gut-Liver Axis Induced by a Dioxin-like Pollutant: An Integrated Metagenomics and Metabolomics Analysis
- Authors
- Hu, C., Liu, M., Wan, T., Tang, L., Sun, B., Zhou, B., Lam, J.C.W., Lam, P.K.S., Chen, L.
- ID
- ZDB-PUB-201229-9
- Date
- 2020
- Source
- Environmental science & technology 55(1): 529-537 (Journal)
- Registered Authors
- Zhou, BingSheng
- Keywords
- none
- MeSH Terms
-
- Animals
- Communication
- Dioxins*
- Environmental Pollutants*
- Female
- Liver
- Male
- Metabolomics
- Metagenomics
- Polychlorinated Biphenyls*
- Zebrafish
- PubMed
- 33356191 Full text @ Env. Sci. Tech.
Citation
Hu, C., Liu, M., Wan, T., Tang, L., Sun, B., Zhou, B., Lam, J.C.W., Lam, P.K.S., Chen, L. (2020) Disturbances in Microbial and Metabolic Communication across the Gut-Liver Axis Induced by a Dioxin-like Pollutant: An Integrated Metagenomics and Metabolomics Analysis. Environmental science & technology. 55(1):529-537.
Abstract
To determine how the aryl hydrocarbon receptor (AhR) signaling acts along the gut-liver axis, we employed an integrated metagenomic and metabolomic approach to comprehensively profile the microbial and metabolic networks. Adult zebrafish were exposed to a model agonist of the AhR: polychlorinated biphenyl (PCB) 126. The metagenomic analysis showed that PCB126 suppressed microbial activities related to primary bile acid metabolism in male intestines. Accordingly, a suite of primary bile acids consistently showed higher concentrations, suggesting that bacterial conversion of primary bile acids was blocked. PCB126 also disturbed bacterial metabolism of bile acids in female intestines, as revealed by higher concentrations of primary bile acids (e.g., chenodeoxycholic acid) and activation of the nuclear farnesoid X receptor signaling. In addition, PCB126 exposure impaired the metabolism of various essential vitamins (e.g., retinol, vitamin B6, and folate). Degradation of vitamin B6 by bacterial enzymes was inhibited in male intestines, resulting in its intestinal accumulation. However, PCB126 suppressed the bacterial metabolism of vitamins in female intestines, causing systematic deficiency of essential vitamins. Overall, we found that PCB126 exposure dysregulated gut microbial activities, consequently interrupting bile acid and vitamin metabolism along the gut-liver axis. The findings provided an insight of the AhR action in microbe-host metabolic communication related to PCBs.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping