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Co-exposure to microcystin-LR and polystyrene nanoplastics aggravates neuroinflammation by promoting AhR/NF-κB axis-mediated gut microbiota dysfunction
Original title: Co-exposure to microcystin-LR and polystyrene nanoplastics aggravates neuroinflammation by promoting AhR/NF-κB axis-mediated gut microbiota dysfunction
Summary
Scientists found that in zebrafish, exposure to two common water pollutants—a toxic algae byproduct (microcystin, found in contaminated lakes) and nanoplastics—together caused worse harm than either alone, damaging gut bacteria balance in a way that triggered brain inflammation and anxiety-like behavior. This matters because it shows how gut health and pollutant exposure can directly affect brain function, and the study found that a common probiotic (Lactobacillus rhamnosus GG) helped reduce this damage, hinting at a possible way to protect against combined pollutant exposure in the future.
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.