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Fragile Guts Make Fragile Brains: Intestinal Epithelial Nrf2 Deficiency Exacerbates Neurotoxicity Induced by Polystyrene Nanoplastics
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Using mice engineered to lack a key protective gene (Nrf2) in their intestinal lining, researchers showed that gut damage from nanoplastics can worsen brain damage through the gut-brain axis. The nanoplastics disrupted the gut barrier, altered gut bacteria, and triggered brain inflammation, with effects being much worse when the gut's natural defenses were weakened -- highlighting how gut health may determine how vulnerable someone is to the neurological effects of plastic pollution.
Oral ingestion is the primary route for human exposure to nanoplastics, making the gastrointestinal tract one of the first and most impacted organs. Given the presence of the gut-brain axis, a crucial concern arises regarding the potential impact of intestinal damage on the neurotoxic effects of nanoplastics (NPs). The intricate mechanisms underlying NP-induced neurotoxicity through the microbiome-gut-brain axis necessitate further investigation. To address this, we used mice specifically engineered with nuclear factor erythroid-derived 2-related factor 2 (Nrf2) deficiency in their intestines, a strain whose intestines are particularly susceptible to polystyrene NPs (PS-NPs). We conducted a 28-day repeated-dose oral toxicity study with 2.5 and 250 mg/kg of 50 nm PS-NPs in these mice. Our study delineated how PS-NP exposure caused gut microbiota dysbiosis, characterized by Mycoplasma and Coriobacteriaceae proliferation, resulting in increased levels of interleukin 17C (IL-17C) production in the intestines. The surplus IL-17C permeated the brain via the bloodstream, triggering inflammation and brain damage. Our investigation elucidated a direct correlation between intestinal health and neurological outcomes in the context of PS-NP exposure. Susceptible mice with fragile guts exhibited heightened neurotoxicity induced by PS-NPs. This phenomenon was attributed to the elevated abundance of microbiota associated with IL-17C production in the intestines of these mice, such as Mesorhizobium and Lwoffii, provoked by PS-NPs. Neurotoxicity was alleviated by in vivo treatment with anti-IL-17C-neutralizing antibodies or antibiotics. These findings advanced our comprehension of the regulatory mechanisms governing the gut-brain axis in PS-NP-induced neurotoxicity and underscored the critical importance of maintaining intestinal health to mitigate the neurotoxic effects of PS-NPs.
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This review summarizes how micro- and nanoplastics may damage the brain through the gut-brain axis, a communication pathway between the digestive system and the nervous system. Nanoplastics can disrupt gut bacteria and weaken the intestinal barrier, potentially sending inflammatory signals to the brain. The authors suggest that targeting gut health could be a way to reduce brain damage caused by nanoplastic exposure.
Microplastics and nano-plastics as emerging gut–brain axis disruptors: mechanistic insights, health implications, and future direction
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This review pulls together existing research showing that the tiny plastic bits we eat and breathe in (microplastics and nanoplastics) can disrupt the healthy bacteria in your gut, weaken your intestinal lining, and trigger inflammation, problems that don't stay put in your stomach. Once this damage occurs, plastic particles and inflammatory signals can travel through the bloodstream and even cross into the brain, potentially contributing to brain inflammation and disrupted brain chemistry. While more research is needed to confirm exact risks in humans, this matters because it suggests everyday plastic exposure could affect not just
Polystyrene nanoplastics trigger ferroptosis in Nrf2-deficient gut via ether phospholipid accumulation
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Researchers discovered that polystyrene nanoplastics trigger a specific type of cell death called ferroptosis in gut lining cells by disrupting fat metabolism, and that mice lacking a key protective protein (Nrf2) in their intestines were especially vulnerable. A high-fat diet made the damage worse, suggesting that people with poor diets or reduced antioxidant defenses may be at greater risk of intestinal harm from nanoplastic exposure.
Oral feeding of nanoplastics affects brain function of mice by inducing macrophage IL-1 signal in the intestine
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Researchers found that when mice consumed nanoplastics, the tiny particles triggered immune cells in the gut to produce an inflammatory signal (IL-1) that traveled to the brain and impaired cognitive function. Nanoplastics were more potent at activating this gut-brain immune pathway than larger microplastics. This study reveals a concerning mechanism by which swallowing nanoplastics in food or water could affect brain health through the gut immune system.
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