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Peer-reviewedCC BYnpj Biofilms and Microbiomes

Intermittent fasting exacerbates microplastic-induced gut inflammation via Rikenella-mediated regulation of purine metabolism and Th17/Treg balance

  • Rui Fu1
  • Yixian Cheng1
  • Junjie Chen1
  • Weiwei Sheng1
  • Jinghua Gu1
  • Jiahao Wang1
  • Zheng Zhang1
  • Huake Cao1
  • Jiawei Zhang1
  • Bo Chen1
  • Guodong Cao1
  1. 1Department of General Surgery, First Affiliated Hospital of Anhui Medical University
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Abstract

The pervasive accumulation of microplastics (MPs) in ecosystems and human bodies has prompted growing concern regarding their biological effects. However, whether intermittent fasting (IF) modulates MP-induced gut injury remains unclear. We established a murine model of chronic oral exposure to 1 μm polystyrene MPs combined with a daily 8-h feeding window. Multi-omics analyses, including 16S rRNA sequencing, untargeted metabolomics, and immune profiling, were performed. In a murine model of chronic oral exposure to 1 μm polystyrene microplastics, IF aggravated colonic inflammation and oxidative stress. 16S rRNA sequencing showed that IF further altered the microplastic-associated gut microbiota, notably reducing Rikenella abundance. Untargeted metabolomics revealed disrupted purine metabolism, including decreased hypoxanthine levels, which positively correlated with Rikenella. Combined MP and IF exposure was associated with an increased Th17/Treg ratio. Supplementation with Rikenella or hypoxanthine partially attenuated inflammatory changes. These findings unveil a previously unappreciated risk of IF under conditions of environmental microplastic exposure, and highlight the necessity of integrating environmental toxicants into evaluations of dietary interventions.

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Cite

BibTeXRIS
BibTeX
@article{fu2026intermittent,
  title = {{Intermittent fasting exacerbates microplastic-induced gut inflammation via Rikenella-mediated regulation of purine metabolism and Th17/Treg balance}},
  author = {Rui Fu and Yixian Cheng and Junjie Chen and Weiwei Sheng and Jinghua Gu and Jiahao Wang and Zheng Zhang and Huake Cao and Jiawei Zhang and Bo Chen and Guodong Cao},
  journal = {npj Biofilms and Microbiomes},
  year = {2026},
  month = jun,
  doi = {10.1038/s41522-026-01016-5},
  url = {https://doi.org/10.1038/s41522-026-01016-5},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Intermittent fasting exacerbates microplastic-induced gut inflammation via Rikenella-mediated regulation of purine metabolism and Th17/Treg balance
AU  - Rui Fu
AU  - Yixian Cheng
AU  - Junjie Chen
AU  - Weiwei Sheng
AU  - Jinghua Gu
AU  - Jiahao Wang
AU  - Zheng Zhang
AU  - Huake Cao
AU  - Jiawei Zhang
AU  - Bo Chen
AU  - Guodong Cao
PY  - 2026
DA  - 2026/06/01
JO  - npj Biofilms and Microbiomes
DO  - 10.1038/s41522-026-01016-5
UR  - https://doi.org/10.1038/s41522-026-01016-5
AB  - The pervasive accumulation of microplastics (MPs) in ecosystems and human bodies has prompted growing concern regarding their biological effects. However, whether intermittent fasting (IF) modulates MP-induced gut injury remains unclear. We established a murine model of chronic oral exposure to 1 μm polystyrene MPs combined with a daily 8-h feeding window. Multi-omics analyses, including 16S rRNA sequencing, untargeted metabolomics, and immune profiling, were performed. In a murine model of chronic oral exposure to 1 μm polystyrene microplastics, IF aggravated colonic inflammation and oxidative stress. 16S rRNA sequencing showed that IF further altered the microplastic-associated gut microbiota, notably reducing Rikenella abundance. Untargeted metabolomics revealed disrupted purine metabolism, including decreased hypoxanthine levels, which positively correlated with Rikenella. Combined MP and IF exposure was associated with an increased Th17/Treg ratio. Supplementation with Rikenella or hypoxanthine partially attenuated inflammatory changes. These findings unveil a previously unappreciated risk of IF under conditions of environmental microplastic exposure, and highlight the necessity of integrating environmental toxicants into evaluations of dietary interventions.
SN  - 2055-5008
ER  -