Dietary Sodium Nitrite Promotes Food Allergy through Dendritic Cell-Mediated Immune Disruption
Although sodium nitrite (SN) is broadly used as a food preservative, its immunomodulatory effects on food allergy pathogenesis remain poorly understood. This study examined how subchronic SN exposure influences dendritic cell (DC)-mediated sensitization and T-cell polarization in an Ovalbumin (OVA)-induced mouse food allergy (FA) model. Our findings reveal that SN exacerbated allergic responses manifested by increased clinical symptoms, reduced weight gain, and elevated serum histamine, MCP-1, and IgE levels compared to those of OVA-sensitization alone. Mechanistically, SN promoted Th2 polarization through T-bet/GATA3 imbalance, Treg suppression, and enhanced DC activation. In vitro studies have demonstrated augmented antigen uptake by SN, MHC II expression, and selectively activated MAPK (p-JNK/ERK1/2) and STAT6 pathways, amplifying Th2 cytokine production and IgE class switching. These findings indicate that SN might disrupt immune homeostasis through coordinated modulation of DC function, Th2 polarization, and regulatory mechanisms, which highlights the potential of SN to exacerbate FA via multiple immunomodulatory pathways.
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