scholarly journals A High-Sodium Diet Modulates the Immune Response of Food Allergy in a Murine Model

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3684
Author(s):  
Zheying Liu ◽  
Shih-Kuan Li ◽  
Chih-Kang Huang ◽  
Ching-Feng Huang

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.

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Rozalia Abramov ◽  
Elizabeth D Drugge ◽  
Khalid A Farhan ◽  
Nicholas R Ferreri

Excessive salt intake is associated with hypertension and cardiovascular morbidity. However, identifying those at risk of salt sensitive hypertension (SSH) remains a challenge due to its unequal distribution among populations and inaccurate assessment of dietary sodium (Na) and potassium (K) intake. The objective of this study was to compare indices of dietary Na intake in relation to systolic blood pressure (SBP) in salt sensitive (SS) and salt resistant (SR) subjects from the Dietary Approaches to Stop Hypertension (DASH)-Sodium trial. We hypothesized that when compared to urinary Na or K independently, Na/K ratio is a better predictor of SSH when defined as a 5-10 mmHg change in SBP from low to high dietary Na. Among 404 Black and White subjects, baseline classifications included 177 SS and 227 SR. After diet randomization, on the control 107 were SS and 92 SR and on the DASH 70 were SS and 135 SR. Descriptive statistics, bivariate analysis, followed by linear regression models for baseline and multilevel mixed-effects models after intervention were used to assess the relationship between SBP and dietary Na (as measured by urinary Na/K ratio or Na and K independently) using SS as a categorical factor. SBP was consistently associated with SS, Na/K ratio, and age in all models . At baseline, SBP was significantly higher in SS and SR subjects of the same race and sex, after controlling for age and urinary Na/K ratio and was highest for White females, SS:142.3 (138.8, 145.7) vs. SR:133.2 (130.7, 135.7), and for Black males, SS:137.0 (133.8, 140.1) vs. SR: 129.6 (127.0, 132.3). On average, SBP increased 1.02 (0.065, 1.98) mmHg with each unit increase in Na/K ratio and 3.30 (2.41, 4.19) mmHg with each 10-year increase in age. After randomization and exposure to increasing levels of sodium, SBP increased in SS subjects on the control diet:125.3 (123.2, 127.3) to 136.8 (134.8, 138.9), an effect that was greater in White vs Black females and in Black vs White males. SBP increased in SS subjects on the DASH diet: 121.4 (118.8, 124.0) to 131.2 (128.7, 133.7), but there were no differences by race and sex. These results suggest that a 5-10 mmHg change in SBP in subjects on a typical American diet and Na/K ratio are good predictors of SSH and that the DASH diet may help to reduce race and sex disparities.


Author(s):  
Christine Y Bakhoum ◽  
Cheryl A M Anderson ◽  
Stephen P Juraschek ◽  
Casey M Rebholz ◽  
Lawrence J Appel ◽  
...  

Abstract BACKGROUND Uromodulin modulates the sodium-potassium-two-chloride transporter in the thick ascending limb of the loop of Henle, and its overexpression in murine models leads to salt-induced hypertension. We hypothesized that individuals with higher baseline levels of urine uromodulin would have a greater increase in systolic blood pressure (SBP) for the same increase in sodium compared with those with lower uromodulin levels. METHODS We used data from 157 subjects randomized to the control diet of the Dietary Approaches to Stop Hypertension (DASH)-Sodium trial who were assigned to 30 days of low (1,500 mg/d), medium (2,400 mg/d), and high salt (3,300 mg/d) diets in random order. Blood pressure was measured prerandomization and then weekly during each feeding period. We evaluated the association of prerandomization urine uromodulin with change in SBP between diets, as measured at the end of each feeding period, using multivariable linear regression. RESULTS Baseline urine uromodulin stratified by tertiles was ≤17.64, 17.65–31.97, and ≥31.98 µg/ml. Across the tertiles, there were no significant differences in SBP at baseline, nor was there a differential effect of sodium diet on SBP across tertiles (low to high, P = 0.81). After adjusting for age, sex, body mass index, and race, uromodulin levels were not significantly associated with SBP change from low to high sodium diet (P = 0.42). CONCLUSIONS In a randomized trial of different levels of salt intake, higher urine uromodulin levels were not associated with a greater increase in blood pressure in response to high salt intake.


Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1970 ◽  
Author(s):  
Grillo ◽  
Salvi ◽  
Coruzzi ◽  
Salvi ◽  
Parati

The close relationship between hypertension and dietary sodium intake is widely recognized and supported by several studies. A reduction in dietary sodium not only decreases the blood pressure and the incidence of hypertension, but is also associated with a reduction in morbidity and mortality from cardiovascular diseases. Prolonged modest reduction in salt intake induces a relevant fall in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group, with larger falls in systolic blood pressure for larger reductions in dietary salt. The high sodium intake and the increase in blood pressure levels are related to water retention, increase in systemic peripheral resistance, alterations in the endothelial function, changes in the structure and function of large elastic arteries, modification in sympathetic activity, and in the autonomic neuronal modulation of the cardiovascular system. In this review, we have focused on the effects of sodium intake on vascular hemodynamics and their implication in the pathogenesis of hypertension.


2021 ◽  
Author(s):  
Sai Sidharth Manikandan ◽  
Murali Dhar

Abstract Background: Non-pharmacological strategies such as lowering sodium intake aim to protect renal function and delay the initiation of renal replacement therapy. It might also be a cost-effective method to improve chronic kidney disease (CKD) prognosis. We decided to perform a meta-analysis of randomized controlled trials (RCTs) to evaluate the effects of low versus high sodium intake in adults with CKD. Results:Our search strategy yielded seven studies from six countries with 465 participants. The overall effect on restricted sodium intake favored reduction in systolic blood pressure with an overall mean difference of -6.14(95% CI: -9.52, -2.76) and reduction in diastolic blood pressure with a mean difference of -3.08 (95% CI: -4.62, -1.55). There was lowering of estimated glomerular filtration rate (eGFR), however the same was not statistically significant.Conclusion:The study found that restricted salt intake could significantly reduce systolic and diastolic BP. Further, multi-center RCTs for longer durations across different stages of CKD could effectively assess the effects of restricted sodium intake on vital parameters. Such study designs could also help clinicians identify the optimal intake of dietary sodium to achieve better renal and cardio vascular outcomes.


2017 ◽  
Vol 66 (5) ◽  
pp. 377-384
Author(s):  
Lianying He ◽  
Lynnette Phillips McCluskey

Lymphatic vessel networks can expand and regress, with consequences for interstitial fluid drainage and nutrient supply to tissues, inflammation, and tumor spread. A diet high in sodium stimulates hyperplasia of cutaneous lymphatic capillaries. We hypothesized that dietary sodium restriction would have the opposite effect, shrinking lymphatic capillaries in the tongue. Lingual lymphatic capillary density and size was significantly reduced in mice fed a low-sodium diet (0.03%) for 3 weeks compared with control-fed mice. Blood vessel density was unchanged. Despite lymphatic capillary shrinkage, lingual edema was not observed. The effect on lymphatic capillaries was reversible, as lymphatic density and size in the tongue were restored by 3 weeks on a control diet. Lymphatic hyperplasia induced by a high-sodium diet is dependent on infiltrating macrophages. However, lingual CD68+ macrophage density was unchanged by sodium deficiency, indicating that distinct mechanisms may mediate lymphatic regression. Further studies are needed to test whether dietary sodium restriction is an effective, non-invasive co-therapy for oral cancer.


1980 ◽  
Vol 59 (1) ◽  
pp. 75-77 ◽  
Author(s):  
H. J. Kramer ◽  
R. Düsing ◽  
H. Stelkens ◽  
R. Heinrich ◽  
J. Kipnowski ◽  
...  

1. In healthy volunteers plasma concentrations of immunoreactive substance P were measured in response to changes in posture and dietary salt intake. 2. In 14 subjects plasma immunoreactive substance P was 168 ± 31 pmol/l when subjects were supine and 401 ± 51 pmol/l (P < 0.001) when they were ambulant. 3. Measurement of supine plasma immunoreactive substance P at 6 h intervals gave a mean value of 240 ± 39 pmol/l at 14.00 hours and a lowest value of 76 ± 9 pmol/l at 02.00 hours. 4. In eight healthy subjects plasma immunoreactive substance P rose only slightly from 169 ± 41 pmol/l, on a sodium intake ad lib., to 244 ± 45 pmol/l by day 4 of dietary sodium restriction (35 mmol/day) and significantly fell to 51 ± 20 pmol/l (P < 0.001) by day 4 of high sodium intake (350 mmol/day). 5. Although exogenous substance P was shown to be natriuretic in dog and rat, the present results do not favour a role of endogenous substance P as a circulating natriuretic factor in man.


2020 ◽  
Vol 33 (5) ◽  
pp. 422-429 ◽  
Author(s):  
Kamila U Migdal ◽  
Matthew C Babcock ◽  
Austin T Robinson ◽  
Joseph C Watso ◽  
Megan M Wenner ◽  
...  

Abstract BACKGROUND High sodium (Na+) intake augments blood pressure variability (BPV) in normotensive rodents, without changes in resting blood pressure (BP). Augmented BPV is associated with end-organ damage and cardiovascular morbidity. It is unknown if changes in dietary Na+ influence BPV in humans. We tested the hypothesis that high Na+ feeding would augment BPV in healthy adults. METHODS Twenty-one participants (10 F/11 M; 26 ± 5 years; BP: 113 ± 11/62 ± 7 mm Hg) underwent a randomized, controlled feeding study that consisted of 10 days of low (2.6 g/day), medium (6.0 g/day), and high (18.0 g/day) salt diets. On the ninth day of each diet, 24-h urine samples were collected and BPV was calculated from 24-h ambulatory BP monitoring. On the tenth day, in-laboratory beat-to-beat BPV was calculated during 10 min of rest. Serum electrolytes were assessed. We calculated average real variability (ARV) and standard deviation (SD) as metrics of BPV. As a secondary analysis, we calculated central BPV from the 24-h ambulatory BP monitoring. RESULTS 24-h urinary Na+ excretion (low = 41 ± 24, medium = 97 ± 43, high = 265 ± 92 mmol/24 h, P &lt; 0.01) and serum Na+ (low = 140.0 ± 2.1, medium = 140.7 ± 2.7, high = 141.7 ± 2.5 mmol/l, P = 0.009) increased with greater salt intake. 24-h ambulatory ARV (systolic BP ARV: low = 9.5 ± 1.7, medium = 9.5 ± 1.2, high = 10.0 ± 1.9 mm Hg, P = 0.37) and beat-to-beat ARV (systolic BP ARV: low = 2.1 ± 0.6, medium = 2.0 ± 0.4, high = 2.2 ± 0.8 mm Hg, P = 0.46) were not different. 24-h ambulatory SD (systolic BP: P = 0.29) and beat-to-beat SD (systolic BP: P = 0.47) were not different. There was a trend for a main effect of the diet (P = 0.08) for 24-h ambulatory central systolic BPV. CONCLUSIONS Ten days of high sodium feeding does not augment peripheral BPV in healthy, adults. CLINICAL TRIALS REGISTRATION NCT02881515.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Joo-Hark Yi ◽  
Mi-yeon Yu ◽  
Jong Wook Choi ◽  
Sang-Woong Han ◽  
Chang Hwa Lee ◽  
...  

Abstract Background and Aims Both high salt diet and abnormal lipid metabolism are critical risks of vascular endothelial dysfunction. This study investigated the interactive effects of increased sodium intake and elevated serum triglyceride (TG) on elevated blood pressure (BP). Method We conducted nation-wide, population-based interaction analysis using Kawasaki method for estimating 24-h urinary sodium excretion (e24hUNaEKawasaki) as a candidate indicator of dietary sodium intake. Eligible as cases were all native Koreans aged 20 years or older without significant medical illness. Results: A total of 16936 participants were divided into quintiles according to their e24hUNaEKawasaki results. Participants in the highest quintile were more obese and hypertensive and had increased white blood cell count, decreased hemoglobin, greater glycemic exposure, and poor lipid profiles as compared to lower quintiles. Linear regression showed that e24UNaEKawasaki was closely related with dietary sodium intake, systolic BP, diastolic BP, and TG. Multiple logistic regression, adjusted for dietary sodium intake and various conventional risk factors of hypertension, demonstrated that both e24UNaEKawasaki and TG were significant predictors of hypertension. Our interaction analysis revealed that high sodium intake had a bigger effect on the risk of hypertension in participants with elevated TG than those without (adjusted RERI = 0.022, 95% CI = 0.017-0.027; adjusted AP = 0.017, 95% CI = 0.006-0.028; adjusted SI = 1.010, 95% CI = 1.007-1.014). Conclusion Our findings indicate that the interaction of high salt diet and abnormal lipid metabolism may exert synergistic biologic effect on the increased arterial BP.


2007 ◽  
Vol 47 (5) ◽  
pp. 544 ◽  
Author(s):  
Dominique Blache ◽  
Micaela J. Grandison ◽  
David G. Masters ◽  
Robyn A. Dynes ◽  
Margaret A. Blackberry ◽  
...  

Grazing saltbush reduces productivity in sheep mostly because the high salt intake decreases feed intake and challenges the metabolism of the animal. However, little is known of the effect of salt load on the endocrine control systems that regulate voluntary feed intake and metabolism. Plasma concentrations of leptin, insulin and cortisol and blood glucose were monitored in wethers fed for 2 weeks with either a control diet (adequate salt) fed ad libitum, a high salt diet (20% of dry matter) fed ad libitum or a group fed the control diet with an intake restricted to that of the high salt ad libitum group (control pair-fed). High salt intakes reduced voluntary feed intake within 1 day and circulating concentrations of insulin and glucose within 2 weeks. Liveweight and leptin concentrations were not specifically affected by the high intake of salt but decreased in response to the decrease in intake. Cortisol secretion was not affected. Although salt intake had a specific effect on insulin and glucose (over and above the effect of reduced feed intake alone), the reduction in insulin would be expected to increase rather than decrease appetite and feed intake. Therefore, insulin, leptin and cortisol do not appear to play major roles in the control of feed intake in sheep consuming high levels of salt.


1995 ◽  
Vol 268 (4) ◽  
pp. F718-F722 ◽  
Author(s):  
E. Folkerd ◽  
D. R. Singer ◽  
F. P. Cappuccio ◽  
N. D. Markandu ◽  
B. Sampson ◽  
...  

We compared endogenous with exogenous lithium clearance (CLi) and studied the effects of dietary salt intake on endogenous CLi in healthy volunteers. Lithium was detectable within a narrow fourfold range in serum and in urine in all 25 subjects studied [serum (n = 25), mean 0.27 +/- 0.02 mumol/l, range 0.13-0.55 mumol/l; urine (n = 20), range 1.49–7.32, mean 4.09 +/- 0.36 mumol/24 h]. Mean clearance and fractional excretion of endogenous lithium were lower (15.2 +/- 2.0 ml/min and 16.4 +/- 2.1%, respectively) compared with results obtained using the exogenous CLi technique (25.5 +/- 1.7 ml/min and 27.9 +/- 2.1%; P < 0.01 and P < 0.05, respectively; n = 17). In a separate group of six normal subjects, absolute (8.7 +/- 2.9 vs. 20.7 +/- 3.8 ml/min) and fractional excretion of lithium (8.3 +/- 2.9 vs. 18.0 +/- 5.1%) were significantly lower on 5 days of low (31 +/- 10 mmol/day) vs. high sodium intake (357 +/- 78 mmol/day; P < 0.05). Use of endogenous CLi precludes the need for lithium tablets. This could be a particular advantage in population studies and permits serial measurement of CLi on different days. Our results show that it is important to take dietary sodium intake into account in studies of endogenous CLi. Lower values for endogenous compared with exogenous CLi could reflect differences in renal handling depending on the plasma lithium concentration. This clearly requires further study.


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