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

Area of Science:

• Environmental Health
• Gastroenterology
• Microbiology

Background:

• Microplastic (MP) accumulation is a growing environmental and health concern.
• The impact of intermittent fasting (IF) on MP-induced gut injury is not well understood.

Purpose of the Study:

• To investigate how IF affects gut injury induced by chronic microplastic exposure in a murine model.
• To explore the underlying mechanisms involving gut microbiota, metabolism, and immune responses.

Main Methods:

• Established a murine model with chronic oral exposure to 1 μm polystyrene MPs and an 8-hour daily feeding window (IF).
• Utilized multi-omics analyses: 16S rRNA sequencing, untargeted metabolomics, and immune profiling.
• Assessed colonic inflammation, oxidative stress, gut microbiota composition, metabolite profiles, and immune cell populations (Th17/Treg ratio).

Main Results:

• Combined MP and IF exposure aggravated colonic inflammation and oxidative stress compared to MP exposure alone.
• IF altered the MP-associated gut microbiota, significantly reducing Rikenella abundance.
• Disrupted purine metabolism was observed, with decreased hypoxanthine levels correlating positively with Rikenella abundance.
• An increased Th17/Treg ratio was associated with combined MP and IF exposure.

Conclusions:

• Intermittent fasting exacerbates microplastic-induced gut injury and inflammation.
• Gut microbiota dysbiosis, particularly reduced Rikenella and altered purine metabolism, plays a role in this exacerbation.
• These findings highlight potential risks of IF in environments with microplastic contamination and the need to consider toxicants in dietary intervention evaluations.