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Microplastic-Induced Disruption of Intestinal Barrier Integrity and Triggering Neuroinflammatory Responses Through Gut-Brain Axis Dysregulation Mediated by NF-κB/PPAR-γ/BDNF Signalling Pathways.
Original title: Microplastic-Induced Disruption of Intestinal Barrier Integrity and Triggering Neuroinflammatory Responses Through Gut-Brain Axis Dysregulation Mediated by NF-κB/PPAR-γ/BDNF Signalling Pathways.
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New research found that when animals were fed common plastic particles (from everyday plastics like grocery bags and food containers) over 45 days, it damaged their gut lining and triggered inflammation that traveled all the way to the brain, along with signs linked to memory problems. This matters because it suggests the tiny plastic bits we're increasingly exposed to through food and water may not just pass through harmlessly — they could disrupt gut health in ways that affect brain function, though more research is needed to confirm this happens in humans.
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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