High-salt diet: HSD, Low-salt diet: LSD, Control diet: CTRL

High-salt diet: HSD, Low-salt diet: LSD, Control diet: CTRL. 3.2. were significantly higher in the HSD group than in the CTRL group (0.001, < 0.05, < 0.01, and < 0.05, respectively). Mice on HSD experienced significantly higher interleukin (IL)-4 levels than the CTRL group (< 0.01). The IL-10 levels were significantly reduced the HSD group than in the CTRL group (< 0.05). The serum levels of interferon- (IFN-), sodium, and chloride did not differ among the three organizations. This study shows that excessive salt intake promotes Th2 reactions inside a mouse model of food allergy. Keywords: food allergy, ovalbumin, IgE, high salt diet, Th2 response 1. Intro Globalization has caused quick changes in peoples eating habits, leading to an increased usage of processed and packaged foods, and a life-style that is based on a high-salt diet (HSD). Excessive salt consumption can present a threat to human being health. High dietary salt intake has been linked to many well-recognized diseases, such as cardiovascular complications, hypertension, and metabolic syndromes [1]. Mounting evidence on the effects of HSD offers demonstrated that it not only mediates hemodynamic changes but also disrupts immune homeostasis. It is well established that excessive salt augments the differentiation of na?ve T cells into T helper 17 cells (Th17), resulting in the onset and exacerbation of autoimmune conditions in animal models of multiple sclerosis, lupus nephritis, rheumatoid arthritis, and Crohns disease [2,3,4]. There is a good balance between Th17 and regulatory T cells (Tregs). Furthermore these T-helper subsets are reciprocally controlled, which enables the transition between pro- and anti-inflammatory claims [5]. Therefore, the enhanced differentiation of Th17 cells after exposure to high concentrations of salt may further dampen Treg phenotypes. Moreover, excessive salt was shown to exert a direct effect within the suppressive functions of Tregs and exacerbate experimental graft-versus-host diseases [6]; Th2 and Tregs also share such a relationship. A change in the equilibrium Efonidipine hydrochloride monoethanolate between allergen-specific Th2 and Treg cells can either result in the development of sensitive diseases or in the recovery from allergy [7,8]. A earlier study demonstrated 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]. Newly found out evidence exposed the epigenetic modifications, caused by decreased or improved levels of histone acetylation at important Th cell loci, contributed to the allergy to cows milk protein or the allergy-protective effect of uncooked milk [10,11]. 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 sensitive diseases, such as food allergies, remains scarce. The manifestation of food allergies is definitely multifactorial and is affected by the Efonidipine hydrochloride monoethanolate genetic background of an individual, environmental factors, and relationships between the genome and environment, including the epigenetic effects. The prevalence of food allergies has been constantly increasing over the last three decades [13]. As evidenced from the epidemiologic studies, up to 10% of the population is affected by food allergies [14]. The present standards for treating food allergy include allergen avoidance and Efonidipine hydrochloride monoethanolate immediate access to medication in the event of anaphylaxis [13]. These are relatively safe and effective actions for controlling symptoms but not for curing the disease. Food allergies are characterized by an overriding Th2 response. The increasing prevalence of food allergies, together with a Efonidipine hydrochloride monoethanolate rise in human being urbanization may Efonidipine hydrochloride monoethanolate show a correlation between the two. Moreover, urbanization prospects to changes in lifestyle and diet is one of the most quick of these changes. The limited evidence within the effect of dietary parts, such as food additives and vitamin D n-3/n-6 polyunsaturated fatty acids, within the homeostasis of the immune system suggests that these parts may hinder or facilitate the development of food allergies [15,16,17]. However, the effect of HSDs or low-salt diet programs (LSDs) on food allergy has not yet been ascertained. Since sodium chloride (NaCl) offers been shown to affect immune homeostasis, we hypothesized that a high salt intake might have an effect on food allergies. Here, we aimed to investigate the effect of dietary salt intake within the immune response inside a mouse model of food allergy. 2. Materials and Methods 2.1. Animals EZR and Ethics Statement Eight-week-old female BALB/c mice were purchased from your National Animal Center (Taipei, Taiwan). All mice were housed in cages under standard conditions of.