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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.
Nanoplastics (NPs) as contaminants in food and water have drawn increasing public attention. However, little is known about how NPs shape the gut immune landscape after injection. In this study, we fabricate NPs (∼500 nm) and microplastics (MPs) (∼2 μm) and evaluate their in vivo effects by feeding them to mice. The results suggest that NPs show a better ability to induce gut macrophage activation than MPs. In addition, NPs trigger gut interleukin-1 (IL-1)-producing macrophage reprogramming via inducing lysosomal damage. More importantly, IL-1 signaling from the intestine can affect brain immunity, leading to microglial activation and Th17 differentiation, all of which correlates with a decline in cognitive and short-term memory in NP-fed mice. Thus, this study provides insight into the mechanism of action of the gut-brain axis, delineates the way NPs reduce brain function, and highlights the importance of fixing the plastic pollution problem worldwide.
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Oral Feeding of Nanoplastics reduces Brain function of Mice by Inducing Intestinal IL-1β-producing Macrophages
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Researchers fabricated nanoplastics (~500 nm) and microplastics (~2 µm) and fed them to mice, using single-cell RNA sequencing of gut and brain tissue to find that nanoplastic oral exposure induced intestinal IL-1β-producing macrophages, which in turn impaired brain function, revealing an indirect gut-immune-brain mechanism of nanoplastic toxicity.
Long-term exposure to polystyrene microplastics reduces macrophages and affects the microbiota–gut–brain axis in mice
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Mice that consumed polystyrene microplastics over an extended period showed reduced immune cells called macrophages in their colons and changes in gut bacteria that were linked to altered brain chemistry. This study provides evidence for a gut-brain connection where microplastics may affect brain function indirectly by first disrupting gut health and the immune system.
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.
Oxidized/unmodified-polyethylene microplastics neurotoxicity in mice: Perspective from microbiota-gut-brain axis
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Mice given polyethylene microplastics by mouth for 28 days showed behavior changes, weakened gut and blood-brain barriers, and inflammation in brain and intestine. Oxidized, weathered particles caused more harm than unmodified ones. Giving Lactobacillus plantarum DP189 with a prebiotic partially reversed the changes in these mice.
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.
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