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Oral exposure to nanoplastics and food allergy in mice fed a normal or high-fat diet
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Researchers studied how oral exposure to polystyrene nanoplastics affects food allergy responses in mice fed either a normal or high-fat diet. They found that nanoplastics worsened allergic reactions to a food protein, particularly in mice on the high-fat diet, by increasing gut permeability and shifting immune responses. The study suggests that the combination of nanoplastic exposure and a Western-style diet may be contributing to the rising prevalence of food allergies.
The global prevalence of food allergies, particularly IgE-mediated responses, is increasing at an alarming rate. This trend is likely driven by environmental factors such as nanoplastics (NPs) ingestion and the westernization of dietary and lifestyle habits. This study examines the impact of polystyrene nanoplastics (PS-NPs) on ovalbumin (OVA)-induced food allergies in mice subjected to either a normal diet (ND) or a high-fat diet (HFD). BALB/c mice were stratified into eight groups based on dietary regimen, NP exposure, and OVA sensitization. Food allergy was induced via OVA administration, and multiple physiological and immunological parameters were evaluated, including body weight, intestinal permeability, cytokine profiles, gut microbiota composition, and small intestinal gene expression. Mice in the HFD + OVA + NP group exhibited significant increases in intestinal permeability, diarrhea severity, and serum OVA-specific IgE levels compared to other groups. Flow cytometric analysis revealed an expansion of innate lymphoid cells (ILC2 and ILC1) within the lamina propria of the small intestine. Shotgun metagenomic sequencing demonstrated gut microbiota dysbiosis, characterized by a reduction in beneficial bacterial populations in the HFD + OVA + NP cohort. Weighted Gene Co-Expression Network Analysis (WGCNA) identified a negative correlation between NPs exposure or OVA sensitization and the expression of Slc1a1, Slc5a8, and Mep1a, while a positive correlation was observed with Aa467197 expression. These findings indicate that oral exposure to PS-NPs exacerbates OVA-induced food allergies, particularly in the context of an HFD, through mechanisms involving increased intestinal permeability, gut microbial dysbiosis, and gene expression modulation. This study highlights the potential health hazards posed by environmental microplastic contamination and its possible contribution to the escalating incidence of food allergies.
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Oral exposure to nano- and microplastics: Potential effects in food allergies?
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This review explored whether exposure to nano- and microplastics through food could contribute to the rising rates of food allergies worldwide. Researchers found that these tiny plastic particles may alter the structure of food allergens, increase gut permeability, promote intestinal inflammation, and disrupt the immune system. While direct evidence is still limited, the study suggests that microplastics in the diet could potentially heighten sensitivity to food allergens.
A Western-style diet shapes the gut and liver responses to low-dose, fit-for-purpose polystyrene nanoplastics in mice
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A subchronic mouse study found that low-dose polystyrene nanoplastics designed to mimic real-world particle characteristics impaired gut and liver health in a non-monotonic, diet-dependent manner, with Western-style diet amplifying the effects.
Polystyrene microplastics exposure increases the disruption of intestinal barrier integrity and gut microbiota homeostasis during obesity and aging
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Researchers found that polystyrene microplastic exposure worsened intestinal barrier dysfunction in mice on high-fat diets, with the combination of obesity and microplastic exposure producing greater gut permeability and inflammation than either factor alone, suggesting compounding risks in metabolically vulnerable individuals.
Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice
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In a mouse study, oral exposure to high concentrations of polystyrene microplastics caused fatty liver disease and abnormal blood lipid levels even without prior gut leakiness. The microplastics triggered intestinal inflammation through immune cells, disrupted gut bacteria, and altered how the body processes nutrients. These results suggest that swallowing microplastics could contribute to metabolic problems and liver disease in humans.
Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.
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A long-term mouse study examined how chronic exposure to polystyrene microspheres interacts with a high-fat diet to affect obesity-related outcomes, finding that microplastics worsened metabolic disruption and fat accumulation compared to diet alone. The results raise concern that microplastic exposure may be an environmental factor contributing to the global obesity epidemic.
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