Oral exposure to nanoplastics and food allergy in mice fed a normal or high-fat diet

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.