High Salt Intake Exacerbates Food Allergy Symptoms by Impairing Intestinal Barrier Function and Activating Mucosal Mast Cells

INTRODUCTION: Recent studies have shown that dietary 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 the influence of high salt intake on 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: non-sensitized/normal diet (CA), non-sensitized/salt diet (CN), sensitized/normal diet (SA), and sensitized/salt diet (SN). CA and SA groups received the AIN-93G diet and water, while CN and SN groups received AIN-93G diet containing 4% NaCl and water containing 1% NaCl ad libitum. Ovalbumin (OVA) sensitization was performed in SA and SN groups on days 7 and 21. 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 mMCP-1 concentrations were evaluated. RESULTS: OVA-specific IgE, IgG1, and IgG2a were significantly elevated in sensitized mice compared with non-sensitized mice, with no additional effect of high salt intake. High salt intake caused a marked reduction in rectal temperature in sensitized mice compared with non-sensitized mice, indicating enhanced anaphylaxis. Sensitized mice fed a high-salt diet also exhibited significantly elevated serum zonulin levels and jejunal villus damage compared with control diet-fed mice. Serum mMCP-1 levels increased with sensitization and were significantly higher in sensitized mice fed a high-salt diet than in sensitized mice fed a control diet. CONCLUSION: High salt intake may worsen food allergy symptoms by disrupting intestinal barrier function and enhancing mucosal mast cell activation.