Dioxin-like polychlorinated biphenyl 126 (PCB126) disrupts gut microbiota-host metabolic dysfunction in mice via aryl hydrocarbon receptor activation

• Published in: Ecotoxicology and environmental safety Vol. 236; p. 113448
• Main Authors: Zhang, Yaran, Cui, Ruina, Shi, Guohui, Dai, Yi, Dong, Jiuhong, Wu, Qi, Zhang, Hongxia, Dai, Jiayin
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01.05.2022; Elsevier
• Subjects: Animals; Aryl hydrocarbon receptor; Bacterial function; Dioxins; Environmental Pollutants - toxicity; Gastrointestinal Microbiome; Gastrointestinal motility; Gut microbiota; Male; Mice; Mice, Inbred C57BL; Polychlorinated biphenyl 126; Polychlorinated Biphenyls - toxicity; Polychlorinated Dibenzodioxins - toxicity; Receptors, Aryl Hydrocarbon - genetics; Receptors, Aryl Hydrocarbon - metabolism; Gut microbiota; Polychlorinated biphenyl 126; Aryl hydrocarbon receptor; Gastrointestinal motility; Bacterial function
• ISSN: 0147-6513; 1090-2414
• DOI: 10.1016/j.ecoenv.2022.113448

Exposure to environmental pollutants, including dioxin-like pollutants, can cause numerous health issues. A common exposure route to pollutants is through contaminated foods, and thus the gastrointestinal system and gut microbiota are often exposed to high amounts of pollutants. Multiple studies have focused on the imbalance in intestinal microbiota composition caused by dioxin-like pollutants. Here, we examined the effects of polychlorinated biphenyl 126 (PCB126) on the composition and functions of gut microbes through metagenomic sequencing, and explored the correlations between microflora dysbiosis and aryl hydrocarbon receptor (AHR) signaling. Adult male wild-type and Ahr-/- mice with a C57BL/6 background were weekly exposed to 50 μg/kg body weight of PCB126 for 8 weeks. Results showed that PCB126 had the opposite effect on gut microbiota composition and diversity in the wild-type and Ahr-/- mice. Functional prediction found that PCB126 exposure mainly altered carbon metabolism and signal regulatory pathways in wild-type mice but impacted DNA replication and lipopolysaccharide biosynthesis in Ahr-/- mice. In wild-type mice, PCB126 exposure induced liver injury, decreased serum lipid content, and delayed gastrointestinal motility, which were significantly correlated to several specific bacterial taxa, such as Helicobacter. Following AHR knockout, however, the holistic effects of PCB126 on the host were lessened or abolished. These results suggest that PCB126 may disrupt host metabolism and gut microbiota dynamics via AHR activation. Overall, our findings provide new insight into the complex interactions between host metabolism and gut microbiota, which may contribute to grouped assessment of environmental pollutants in the future. [Display omitted] •PCB126 exposure altered gut microbiota composition and function in mice.•PCB126-induced gut microbiota dysbiosis associated with AHR signal pathway.•PCB126 exposure delayed gastrointestinal motility in an AHR-dependent manner.•Specific bacterial taxa significantly correlated with dyslipidemia and gut motility.