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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
Plastics are synthetic polymers widely used for their versatility, longer shelf life, and low cost. However, the non-biodegradable nature of conventional plastics has led to accumulation of microplastics (MPs; <5mm) and nanoplastics (NPs; <100 nm) in aquatic, terrestrial, and atmospheric environments. MNPs are composed of polyethene, polypropylene, polystyrene, polyvinyl chloride, and polyethene terephthalate. Human exposure to micro and nanoplastics occurs mainly through ingestion, inhalation, and rarely through dermal contact. The gastrointestinal tract is the potential accumulation site for such particles, which leads to microbial dysbiosis, disturbs intestinal barrier integrity and induces oxidative stress and inflammation. These disruptions lead to diseases related to the gastrointestinal tract, chronic systemic inflammation and affect the gut-brain axis with neuroinflammatory consequences. This review highlights gut dysbiosis and intestinal barrier disruption as a crucial gateway mediating the systemic effects of MNPs. On exposure to MNPs, gut microbial composition is altered by reducing beneficial short-chain fatty acid-producing bacteria such as Faecalibacterium, Roseburia , and Bifidobacterium , while stimulating the growth of opportunistic pathogens such as Desulfovibrio spp. Subsequent reductions in short-chain fatty acid generation induce lipopolysaccharide release and downregulation of tight junction proteins that compromise intestinal barrier integrity and expedite the translocation of MNPs, microbial products, and pro-inflammatory determinants into systemic circulation. MNPs then cross the blood-brain barrier by receptor-mediated routes, paracellular diffusion, or transcytosis, which is exacerbated by inflammation and oxidative stress. Excessive ROS further cause mitochondrial dysfunction, neuroinflammation, microglial activation, neurotransmitter imbalance, and pathological protein aggregation. This is a narrative review, focusing on integrating current evidence on the role of MNPs in disturbing the gut-brain axis through gut dysbiosis, intestinal barrier dysfunction, increased oxidative stress, inflammation, and altered neurochemical signaling. It further highlights the consequences of these changes in systemic health, identifies key knowledge gaps, and outlines future research priorities to better understand and mitigate the health risks.
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Ingested microplastics and the gut–brain axis: A systematic review of mechanistic pathways and neurobiological impacts in human and preclinical models
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This review summarizes existing research on tiny plastic particles and the gut-brain connection in rodent and human cell studies. Swallowed or inhaled plastics built up in the digestive tract, altered gut bacteria, and were linked to inflammation and behavior changes in animals. In rodent studies, treatments like fecal transplants and certain probiotics were linked to reduced brain-related harm from plastic exposure.
Micro- and nanoplastics and potential perturbation of the microbiota-gut-brain axis.
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This review summarizes existing research on microplastics and nanoplastics and their possible effects on the gut, its microbes, and the brain. Animal studies found changes in gut bacteria, gut barrier function, inflammation, and behavior, but human evidence remains limited and cannot yet show these particles cause brain disease.
Innovative mechanisms of micro- and nanoplastic-induced brain injury: Emphasis on the microbiota-gut-brain axis
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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.
Nanoplastic Impact on the Gut-Brain Axis: Current Knowledge and Future Directions
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Researchers reviewed the emerging evidence on how nanoplastics may affect the gut-brain axis, the communication pathway between the digestive and nervous systems. Studies indicate that nanoplastic exposure can alter gut microbiota, increase intestinal permeability, trigger oxidative stress and inflammation, and produce neurotoxic and behavioral effects. The review calls for more research given the ubiquitous presence of plastics in the human environment and the potential for nanoplastics to disrupt this critical biological communication pathway.
Micro- and nanoplastics disrupt the gut–liver–brain axis: mechanisms of multi-organ toxicity in animal models
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This review pulls together animal research showing that tiny plastic particles (micro- and nanoplastics) don't just pass through your body harmlessly—they can damage the gut lining, throw off gut bacteria, and trigger inflammation that spreads to the liver and even the brain. The smallest particles (nanoplastics) seem especially good at slipping past the body's protective barriers, raising concern about their effects on human health. Since this is based on animal studies so far, more research is needed to confirm how directly these findings apply to people, but it strengthens the case that everyday plastic exposure deserves closer attention.
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