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High Salt Intake Exacerbates Food Allergy Symptoms by Impairing Intestinal Barrier Function and Activating Mucosal
Suzuno Ota1, Hibiki Yamaguchi1, Sayaka Yokoyama1,2
1Graduate School of Bioscience and Biotechnology, Chubu University, Kasugai, Japan.
Introduction:
Recent studies have shown that salt affects the differentiation and function of T helper cell subsets; however, its influence on food allergies and the underlying mechanisms remains unclear. This study aimed to clarify how high salt intake exacerbates allergic responses by examining its effects on immune function and intestinal barrier integrity in a food allergy mouse model.
Methods:
Five-week-old female BALB/c mice were assigned to four groups: Control/AIN-93 G diet group (CA), Control/NaCl diet group (CN), Sensitization/AIN-93 G diet group (SA), and Sensitization/NaCl diet group (SN). CA and SA groups received the AIN-93 G diet and water, while CN and SN groups received AIN-93 G containing 4% NaCl and 1% NaCl water ad libitum. Ovalbumin (OVA) sensitization was performed in SA and SN groups. On day 28, OVA was administered orally. Rectal temperature, serum, and jejunal samples were collected 30 min later. Anaphylaxis severity, OVA-specific antibody responses, serum zonulin levels, jejunal histology, and serum mouse mast cell protease-1 (mMCP-1) concentrations were evaluated.
Results:
OVA-specific IgE, IgG1, and IgG2a were significantly elevated by sensitization, with no additional effects of salt intake. Salt loading caused a marked reduction in rectal temperature in the SN group, indicating enhanced anaphylaxis. The SN group also exhibited elevated serum zonulin levels and villus damage. Serum mMCP-1 increased with sensitization and was highest in the SN group.
Conclusion:
High salt intake may worsen food allergy symptoms by disrupting intestinal barrier function and enhancing mucosal mast cell activation.
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