Environment internationalJun 11, 2026

Combined exposure to microcystin-LR and tiny plastic particles worsens brain inflammation by disrupting gut bacteria through the AhR/NF-κB pathway

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Jun 12, 2026

Abstract

Exposure to 25 μg/L microcystin-LR and 1 mg/L polystyrene nanoplastics together for 30 days caused significant gut-brain axis disruptions in adult zebrafish.

Co-exposure to microcystin-LR and polystyrene nanoplastics disrupted gut microbiota balance, which is linked to increased brain inflammation.
Microcystin-LR alone caused intestinal damage and structural changes, while polystyrene nanoplastics intensified these effects, worsening gut barrier integrity.
The combination of these contaminants allowed harmful substances from the gut to enter the brain, potentially increasing neuroinflammation.
A decrease in beneficial bacteria Lactobacillus and an increase in harmful bacteria Desulfovibrionaceae were observed, impacting tryptophan metabolism.
The imbalance in gut microbiota was associated with heightened neuroinflammation and abnormal neuronal development.
Supplementation with probiotics Lactobacillus rhamnosus GG was found to reduce neuroinflammation linked to the combined exposure.

Simplified

Microcystin-LR (MC-LR) and polystyrene nanoplastics (PS-NP) are common aquatic contaminants known to cause intestinal and neural toxicity in fish. However, their combined toxic effects and the role of gut-brain interactions are not well understood. Here, adult zebrafish were exposed to 1, 25 μg/L MC-LR and 1 mg/L PS-NP alone or in combination for 30 days to assess their toxicities. Mechanistically, co-exposure to MC-LR and PS-NP perturbed gut microbiota homeostasis, which mediated brain lesions and inflammation, manifesting as pronounced anxiety-like behavior via the gut-brain axis. Notably, MC-LR exposure induced intestinal damage and structural alterations, while PS-NP co-treatment exacerbated the disruption of intestinal barrier integrity and heightened gut inflammation. The impaired intestinal and blood-brain barrier allowed gut-derived lipopolysaccharide (LPS) to reach the brain, increasing inflammation and harming brain health. PS-NP worsen MC-LR toxicity by disrupting gut microbiota balance, reducing beneficial bacteria Lactobacillus, and increasing harmful bacteria Desulfovibrionaceae, which led to substantial disturbances in microbiota-derived tryptophan metabolism. This imbalance suppressed aryl hydrocarbon receptor (AhR) expression and activated the NF-κB signaling pathway with the brain, further intensifying neuroinflammation and abnormal neuronal development. In addition, supplementation with probiotics, Lactobacillus rhamnosus GG (LGG), can mitigate neuroinflammation induced by the combined exposure by remodeling gut microbiota. The study indicated that gut microbiota plays a key role in the intestine-brain communication, influencing neurotoxicity from combined MC-LR and PS-NP exposure. It elucidates how microcystins and nanoplastics jointly disrupt this axis and suggests a promising strategy for counteracting their combined toxic effects.

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Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

PubMed

Combined exposure to microcystin-LR and tiny plastic particles worsens brain inflammation by disrupting gut bacteria through the AhR/NF-κB pathway

Abstract

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Abstract

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