scholarly journals High-salt diet mediates interplay between NK cells and gut microbiota to induce potent tumor immunity

2021 ◽  
Vol 7 (37) ◽  
Author(s):  
Zaigham Abbas Rizvi ◽  
Rajdeep Dalal ◽  
Srikanth Sadhu ◽  
Yashwant Kumar ◽  
Shakti Kumar ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Nk Cells ◽  
Tumor Immunity ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Potent Tumor

Calcitriol ameliorates damage in high-salt diet-induced hypertension: Evidence of communication with the gut–kidney axis

2021 ◽  
pp. 153537022110625
Author(s):  
Ruifeng Ding ◽  
Zilong Xiao ◽  
Yufeng Jiang ◽  
Yi Yang ◽  
Yang Ji ◽  
...  
Keyword(s):  
Vitamin D ◽  
Gut Microbiota ◽  
Intestinal Flora ◽  
Intestinal Barrier ◽  
Vitamin D Supplementation ◽  
High Salt ◽  
Intestinal Barrier Function ◽  
High Salt Diet ◽  
Salt Diet ◽  
Induced Hypertension

Several studies have established a link between high-salt diet, inflammation, and hypertension. Vitamin D supplementation has shown anti-inflammatory effects in many diseases; gut microbiota is also associated with a wide variety of cardiovascular diseases, but potential role of vitamin D and gut microbiota in high-salt diet-induced hypertension remains unclear. Therefore, we used rats with hypertension induced by a high-salt diet as the research object and analyzed the transcriptome of their tissues (kidney and colon) and gut microbiome to conduct an overall analysis of the gut–kidney axis. We aimed to confirm the effects of high salt and calcitriol on the gut–kidney immune system and the composition of the intestinal flora. We demonstrate that consumption of a high-salt diet results in hypertension and inflammation in the colon and kidney and alteration of gut microbiota composition and function. High-salt diet-induced hypertension was found to be associated with seven microbial taxa and mainly associated with reduced production of the protective short-chain fatty acid butyrate. Calcitriol can reduce colon and kidney inflammation, and there are gene expression changes consistent with restored intestinal barrier function. The protective effect of calcitriol may be mediated indirectly by immunological properties. Additionally, the molecular pathways of the gut microbiota-mediated blood pressure regulation may be related to circadian rhythm signals, which needs to be further investigated. An innovative association analysis of the microbiota may be a key strategy to understanding the association between gene patterns and host.

Su1901 High Salt Diet Increases Susceptibility to Experimental Colitis: A Putative Role of Gut Microbiota

2016 ◽  
Vol 150 (4) ◽  
pp. S583 ◽  
Author(s):  
Pedro M. Miranda ◽  
Viktoria Serkis ◽  
Giada de Palma ◽  
Marc Pigrau ◽  
Jun Lu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Experimental Colitis ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Putative Role

scholarly journals High-Salt Diet Has a Certain Impact on Protein Digestion and Gut Microbiota: A Sequencing and Proteome Combined Study

2017 ◽  
Vol 8 ◽  
Author(s):  
Chao Wang ◽  
Zixin Huang ◽  
Kequan Yu ◽  
Ruiling Ding ◽  
Keping Ye ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Salt ◽  
Protein Digestion ◽  
High Salt Diet ◽  
Salt Diet

scholarly journals Berry-Enriched Diet in Salt-Sensitive Hypertensive Rats: Metabolic Fate of (Poly)Phenols and the Role of Gut Microbiota

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2634 ◽  
Author(s):  
Gomes ◽  
Oudot ◽  
Macià ◽  
Foito ◽  
Carregosa ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Salt ◽  
In Vivo Model ◽  
Microbiota Composition ◽  
Metabolic Fate ◽  
Hypertensive Rats ◽  
High Salt Diet ◽  
16S Rrna Analysis ◽  
Salt Diet

Diets rich in (poly)phenols are associated with a reduced reduction in the incidence of cardiovascular disorders. While the absorption and metabolism of (poly)phenols has been described, it is not clear how their metabolic fate is affected under pathological conditions. This study evaluated the metabolic fate of berry (poly)phenols in an in vivo model of hypertension as well as the associated microbiota response. Dahl salt-sensitive rats were fed either a low-salt diet (0.26% NaCl) or a high-salt diet (8% NaCl), with or without a berry mixture (blueberries, blackberries, raspberries, Portuguese crowberry and strawberry tree fruit) for 9 weeks. The salt-enriched diet promoted an increase in the urinary excretion of berry (poly)phenol metabolites, while the abundance of these metabolites decreased in faeces, as revealed by UPLC–MS/MS. Moreover, salt and berries modulated gut microbiota composition as demonstrated by 16S rRNA analysis. Some changes in the microbiota composition were associated with the high-salt diet and revealed an expansion of the families Proteobacteria and Erysipelotrichaceae. However, this effect was mitigated by the dietary supplementation with berries. Alterations in the metabolic fate of (poly)phenols occur in parallel with the modulation of gut microbiota in hypertensive rats. Thus, beneficial effects of (poly)phenols could be related with these interlinked modifications, between metabolites and microbiota environments.

Targeting the Gut Microbiota to Investigate the Mechanism of Lactulose in Negating the Effects of a High‐Salt Diet on Hypertension

2019 ◽  
Vol 63 (11) ◽  
pp. 1800941 ◽  
Author(s):  
Zheng Zhang ◽  
Jiangtao Zhao ◽  
Changyu Tian ◽  
Xiao Chen ◽  
Huan Li ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet

scholarly journals A High-Salt Diet Disturbs the Development and Function of Natural Killer Cells in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Xiaokang Zeng ◽  
Yan Li ◽  
Weibiao Lv ◽  
Xinhuai Dong ◽  
Chong Zeng ◽  
...  
Keyword(s):  
Nk Cells ◽  
Natural Killer ◽  
Molecular Mechanism ◽  
Nk Cell ◽  
Cell Subset ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Ifn Γ ◽  
And Function

A high-salt diet (HSD) is common worldwide and can lead to cardiovascular disease, chronic inflammation, and autoimmune diseases. Moreover, increasing evidence shows that HSD is closely related to a variety of immune diseases. Natural killer (NK) cells are important innate immune cells that directly kill their targets via degranulation and secretion of interferon gamma (IFN-γ). NK cells play a vital role in resisting viruses and preventing the malignant transformation of cells; however, whether HSD affects the development and function of NK cells has not yet been elucidated. Therefore, the purpose of the present study was to understand the effects of HSD on the development and function of NK cells, in addition to investigating the underlying molecular mechanism. Our results show that the number of NK cells in the spleen and lungs of HSD-fed mice was significantly reduced, which may be due to the inhibition of NK cell proliferation. Further, the development of NK cells in mice was evaluated, and it was found that HSD reduced the effective NK cell subset (CD27+CD11b-). Moreover, it was also found that the ability of NK cells to secrete CD107a and IFN-γ in HSD-fed mice was decreased following stimulation with RMA-S and YAC-1 tumor cells. Finally, the underlying molecular mechanism was evaluated, and it was found that HSD increased the production of reactive oxygen species (ROS) by NK cells, while the expression of CD122 was decreased, suggesting that HSD downregulates CD122 expression in NK cells via ROS signaling, thereby reducing the responsiveness to IL-15 and ultimately inhibiting NK cell function. The present research discovered a novel mechanism by which HSD inhibits the function of NK cells, providing an alternative avenue for the treatment of immune diseases caused by HSD.

463-P: Deterioration of Atherosclerosis via Dysbiosis in ApoE Null Mice Fed with High-Salt Diet

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 463-P
Author(s):  
TOMONORI KIMURA ◽  
YOSHITAKA HASHIMOTO ◽  
TAKAFUMI SENMARU ◽  
EMI USHIGOME ◽  
MASAHIDE HAMAGUCHI ◽  
...  
Keyword(s):  
High Salt ◽  
High Salt Diet ◽  
Salt Diet

scholarly journals Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

2019 ◽  
Vol 20 (14) ◽  
pp. 3495 ◽  
Author(s):  
Yanling Yan ◽  
Jiayan Wang ◽  
Muhammad A. Chaudhry ◽  
Ying Nie ◽  
Shuyan Sun ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Significant Rise ◽  
Protein Carbonylation ◽  
High Salt ◽  
Kidney Cortex ◽  
High Salt Diet ◽  
Salt Diet ◽  
Salt Sensitive Hypertension

We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.

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