Molecular neurobiologyJul 6, 2026

Microplastics harm the gut lining and may cause brain inflammation by disrupting gut-brain communication through key cell signaling pathways

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Jul 7, 2026

Abstract

Exposure to 10 and 100 mg/kg BW of polyethylene and polypropylene microplastics for 45 days significantly disrupted intestinal barrier integrity.

Intestinal barrier integrity was compromised, evidenced by reduced expression of zonula occludens-1.
Exposure led to altered short-chain fatty acid profiles, indicating impaired gut microbial activity.
Increased oxidative stress was observed, marked by reduced antioxidant defense and heightened lipid peroxidation.
Elevated inflammatory mediators and altered neurochemical markers were detected in both small intestine and brain tissues.
Behavioral abnormalities and histopathological changes were noted, suggesting neuroinflammatory toxicity linked to gut-brain axis dysregulation.
Polyethylene microplastics caused more severe toxic effects compared to polypropylene microplastics, especially at the higher dose.

Simplified

Microplastics (MPs) are emerging environmental contaminants increasingly implicated in intestinal dysfunction and neuroinflammatory alterations through gut-brain axis (GBA) dysregulation. However, the mechanistic involvement of polyethylene (PE) and polypropylene (PP) MPs in GBA-associated neurotoxicity remains insufficiently understood. Therefore, the present study aimed to evaluate the impact of PE- and PP-MPs on intestinal barrier integrity, oxidative stress, neuroinflammation, and synaptic dysfunction. Following physicochemical characterization, experimental animals were orally exposed to PE- and PP-MPs (10 and 100 mg/kg BW) for 45 consecutive days. MP exposure significantly disrupted intestinal barrier integrity, reduced zonula occludens-1 expression, and altered short-chain fatty acid profiles, indicating impaired gut microbial metabolic activity. Concurrently, oxidative stress and inflammatory responses were evidenced by reduced antioxidant defence, increased lipid peroxidation, elevated inflammatory mediators, and altered neurochemical markers in small intestine and brain tissues. Behavioral abnormalities, increased amyloid precursor protein (APP) expression, tau-associated pathological alterations, and histopathological changes further indicated GBA impairment following MP exposure. Notably, PE-MPs produced comparatively greater toxicological effects than PP-MPs, particularly at higher dose. Overall, the findings demonstrate that chronic exposure to environmentally relevant PE- and PP-MPs disrupts intestinal homeostasis and promotes neuroinflammatory toxicity through GBA dysregulation.

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Competing interests

Declarations. Ethical Approval: This work has received approval of the experimental protocols by the Institutional Animal Ethics Committee (1972/PH/BIT/93/24/IAEC) and the certificate of approval is available upon request. Competing interests: The authors declare no competing interests.

PubMed

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Microplastics harm the gut lining and may cause brain inflammation by disrupting gut-brain communication through key cell signaling pathways

Abstract

Full Text

Funding

Competing interests

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