Abstract
Mounting evidence demonstrates that a high-salt diet (HSD) not only affects hemodynamic changes but also disrupts immune homeostasis. The T helper 17 (Th17) and regulatory T cells (Tregs) are susceptible to hypersalinity. However, research on the influence of sodium on Th2-mediated food allergies remains scarce. We aimed to investigate the effect of dietary sodium on the immune response to food allergies. Mice maintained on an HSD (4% NaCl), low-salt diet (LSD; 0.4% NaCl), or control diet (CTRL; 1.0% NaCl) were orally sensitized with ovalbumin (OVA) and a cholera toxin (CT) adjuvant, and then subjected to an intragastric OVA challenge. OVA-specific immunoglobulin G (IgG), IgG1, IgG2a, and IgE antibodies were significantly higher in the HSD group than in the CTRL group (p < 0.001, p < 0.05, p < 0.01, and p < 0.05, respectively). Mice on HSD had significantly higher interleukin (IL)-4 levels than the CTRL group (p < 0.01). The IL-10 levels were significantly lower in the HSD group than in the CTRL group (p < 0.05). The serum levels of interferon-γ (IFN-γ), sodium, and chloride did not differ among the three groups. This study indicates that excessive salt intake promotes Th2 responses in a mouse model of food allergy.
Highlights
Globalization has caused rapid changes in people’s eating habits, leading to an increased consumption of processed and packaged foods, and a lifestyle that is based on a high-salt diet (HSD)
IgE serum antibodies between the low-salt diet (LSD) and control diet (CTRL) groups
The concentration of IL-4 was significantly higher in the HSD group than in the CTRL group, after the stimulation with OVA (p < 0.01 for Figure 3a)
Summary
Globalization has caused rapid changes in people’s eating habits, leading to an increased consumption of processed and packaged foods, and a lifestyle that is based on a high-salt diet (HSD). Excessive salt was shown to exert a direct effect on the suppressive functions of Tregs and exacerbate experimental graft-versus-host diseases [6]; Th2 and Tregs share such a relationship. A previous study demonstrated that the failure to induce oral tolerance, or the breakdown of oral tolerance as a result of the impaired generation or functioning of the suppressive Tregs, could contribute to food allergy [9]. While it is well known that sodium is an immunomodulator of Th17 cells and Tregs [12], our understanding of the direct effect of sodium on Th2-dependent allergic diseases, such as food allergies, remains scarce
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