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Published on: July 27, 2022
Polydisperse polystyrene microplastics exacerbate colitis through gut microbiota-butyrate-PPARγ axis disruption in
Zhian Zhai1, Ying Yang1, Yifei Xu1
1State Key Laboratory of Animal Nutrition and Feeding, Department of Companion Animal Science, China Agricultural University, Beijing 100193, China.
Abstract:
The escalating global prevalence of inflammatory bowel disease (IBD) parallels widespread dietary exposure to microplastics (MPs), yet causal mechanisms linking polydisperse MPs to colitis remain elusive. Here, we show that polydisperse polystyrene microspheres (PS-MS) exacerbate dextran sulfate sodium (DSS)-induced colitis in mice by disrupting a microbiota-butyrate-PPARγ signaling axis. Mechanistically, PS-MS treatment alone does not directly induce colon inflammation in healthy mice; however, it suppresses intestinal Muc2 protein expression and impairs the mucus barrier by reducing the abundance of Lachnospiraceae_NK4A136_group and butyrate levels, thereby inhibiting PPARγ signaling and aggravating colitis. An antibiotic cocktail (ABX)-mediated microbiota ablation abolishes PS-MS-induced colitis aggravation, whereas fecal microbiota transplantation (FMT) from PS-MS-exposed donors transmits susceptibility to antibiotic-treated mice, confirming microbiota-dependent pathogenesis. Exogenous sodium butyrate supplementation restores mucosal homeostasis via PPARγ activation, as evidenced by the abolition of protection following administration of the PPARγ antagonist GW9662, and by the comparable efficacy of the PPARγ agonist 5-ASA. Our findings establish the microbiota-butyrate-PPARγ axis as a critical target for counteracting the adverse effects of environmental MPs and propose butyrate-boosting therapies as a translatable strategy against IBD.
Insights
Microplastics (MPs) worsen inflammatory bowel disease (IBD) by disrupting gut bacteria and butyrate production, impairing a key signaling pathway. Restoring butyrate levels may offer a therapeutic strategy against MP-induced colitis.
Area of Science:
- Environmental Health
- Gastroenterology
- Microbiology
Background:
- Rising global inflammatory bowel disease (IBD) rates coincide with increased microplastic (MP) exposure.
- The precise mechanisms by which MPs contribute to colitis are not fully understood.
Purpose of the Study:
- To investigate how polydisperse MPs influence dextran sulfate sodium (DSS)-induced colitis in a mouse model.
- To elucidate the role of the gut microbiota, butyrate, and PPARγ signaling in MP-induced exacerbation of colitis.
Main Methods:
- Mice were treated with polydisperse polystyrene microspheres (PS-MS) and DSS to induce colitis.
- Microbiota manipulation using antibiotic cocktails (ABX) and fecal microbiota transplantation (FMT) were employed.
- Mucus barrier integrity, Lachnospiraceae_NK4A136_group abundance, and butyrate levels were assessed.
- PPARγ signaling was evaluated using agonists (5-ASA) and antagonists (GW9662), alongside exogenous sodium butyrate supplementation.
Main Results:
- PS-MS exacerbated DSS-induced colitis by disrupting the microbiota-butyrate-PPARγ axis.
- PS-MS suppressed intestinal Muc2 expression and impaired the mucus barrier by reducing butyrate-producing bacteria and butyrate levels.
- Microbiota ablation prevented PS-MS-induced colitis aggravation, while FMT transmitted susceptibility, confirming microbiota-dependent pathogenesis.
- Sodium butyrate supplementation restored mucosal homeostasis via PPARγ activation, demonstrating therapeutic potential.
Conclusions:
- Polydisperse MPs aggravate colitis through a microbiota-dependent disruption of the butyrate-PPARγ signaling axis.
- Targeting the microbiota-butyrate-PPARγ axis presents a viable therapeutic strategy for mitigating MP-associated IBD.
- Butyrate-boosting therapies offer a translatable approach for managing IBD exacerbated by environmental MPs.
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