scholarly journals Helicobacter pylori AdaptationIn Vivoin Response to a High-Salt Diet

2015 ◽  
Vol 83 (12) ◽  
pp. 4871-4883 ◽  
Author(s):  
John T. Loh ◽  
Jennifer A. Gaddy ◽  
Holly M. Scott Algood ◽  
Silvana Gaudieri ◽  
Simon Mallal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Helicobacter Pylori ◽  
High Salt ◽  
Mongolian Gerbils ◽  
High Salt Diet ◽  
Salt Diet ◽  
Content Type ◽  
Regular Diet ◽  
H Pylori ◽  
And Oxidative Stress

Helicobacter pyloriexhibits a high level of intraspecies genetic diversity. In this study, we investigated whether the diversification ofH. pyloriis influenced by the composition of the diet. Specifically, we investigated the effect of a high-salt diet (a known risk factor for gastric adenocarcinoma) onH. pyloridiversification within a host. We analyzedH. pyloristrains isolated from Mongolian gerbils fed either a high-salt diet or a regular diet for 4 months by proteomic and whole-genome sequencing methods. Compared to the input strain and output strains from animals fed a regular diet, the output strains from animals fed a high-salt diet produced higher levels of proteins involved in iron acquisition and oxidative-stress resistance. Several of these changes were attributable to a nonsynonymous mutation infur(fur-R88H). Further experiments indicated that this mutation conferred increased resistance to high-salt conditions and oxidative stress. We propose a model in which a high-salt diet leads to high levels of gastric inflammation and associated oxidative stress inH. pylori-infected animals and that these conditions, along with the high intraluminal concentrations of sodium chloride, lead to selection ofH. pyloristrains that are most fit for growth in this environment.

scholarly journals High Dietary Salt Intake Exacerbates Helicobacter pylori-Induced Gastric Carcinogenesis

2013 ◽  
Vol 81 (6) ◽  
pp. 2258-2267 ◽  
Author(s):  
Jennifer A. Gaddy ◽  
Jana N. Radin ◽  
John T. Loh ◽  
Feng Zhang ◽  
M. Kay Washington ◽  
...  
Keyword(s):  
Mutant Strain ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Content Type ◽  
Dietary Salt Intake ◽  
Regular Diet ◽  
H Pylori

ABSTRACTPersistent colonization of the human stomach withHelicobacter pyloriis a risk factor for gastric adenocarcinoma, andH. pylori-induced carcinogenesis is dependent on the actions of a bacterial oncoprotein known as CagA. Epidemiological studies have shown that high dietary salt intake is also a risk factor for gastric cancer. To investigate the effects of a high-salt diet, we infected Mongolian gerbils with a wild-type (WT)cagA+H. pyloristrain or an isogeniccagAmutant strain and maintained the animals on a regular diet or a high-salt diet. At 4 months postinfection, gastric adenocarcinoma was detected in 100% of the WT-infected/high-salt-diet animals, 58% of WT-infected/regular-diet animals, and none of the animals infected with thecagAmutant strain (P< 0.0001). Among animals infected with the WT strain, those fed a high-salt diet had more severe gastric inflammation, higher gastric pH, increased parietal cell loss, increased gastric expression of interleukin 1β (IL-1β), and decreased gastric expression of hepcidin and hydrogen potassium ATPase (H,K-ATPase) compared to those on a regular diet. Previous studies have detected upregulation of CagA synthesis in response to increased salt concentrations in the bacterial culture medium, and, concordant with thein vitroresults, we detected increasedcagAtranscriptionin vivoin animals fed a high-salt diet compared to those on a regular diet. Animals infected with thecagAmutant strain had low levels of gastric inflammation and did not develop hypochlorhydria. These results indicate that a high-salt diet potentiates the carcinogenic effects ofcagA+H. pyloristrains.

scholarly journals Hsp90β is involved in the development of high salt-diet-induced nephropathy via interaction with various signalling proteins

Open Biology ◽  
2016 ◽  
Vol 6 (4) ◽  
pp. 150159 ◽  
Author(s):  
Shi-hai Yan ◽  
Ning-wei Zhao ◽  
Wei-min Jiang ◽  
Xin-tong Wang ◽  
Si-qi Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Salt ◽  
Shr Rats ◽  
High Salt Diet ◽  
Salt Loading ◽  
Salt Diet ◽  
Cellular Signalling ◽  
Signalling Cascades ◽  
Wistar Kyoto ◽  
And Oxidative Stress

A high-salt diet often leads to a local intrarenal increase in renal hypoxia and oxidative stress, which are responsible for an excess production of pathogenic substances. Here, Wistar Kyoto/spontaneous hypertensive (WKY/SHR) rats fed a high-salt diet developed severe proteinuria, resulting from pronounced renal inflammation, fibrosis and tubular epithelial cell apoptosis. All these were mainly non-pressure-related effects. Hsp90β, TGF-β, HIF-1α, TNF-α, IL-6 and MCP-1 were shown to be highly expressed in response to salt loading. Next, we found that Hsp90β might play the key role in non-pressure-related effects of salt loading through a series of cellular signalling events, including the NF-κB, p38 activation and Bcl-2 inactivation. Hsp90β was previously proven to regulate the upstream mediators in multiple cellular signalling cascades through stabilizing and maintaining their activities. In our study, 17-dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG) or Hsp90β knockdown dramatically alleviated the high-salt-diet-induced proteinuria and renal damage without altering blood pressure significantly, when it reversed activations of NF-κB, mTOR and p38 signalling cascades. Meanwhile, Co-IP results demonstrated that Hsp90β could interact with and stabilize TAK1, AMPKα, IKKα/β, HIF-1α and Raptor, whereas Hsp90β inhibition disrupted this process. In addition, Hsp90β inhibition-mediated renal improvements also accompanied the reduction of renal oxidative stress. In conclusion, salt loading indeed exhibited non-pressure-related impacts on proteinuria and renal dysfunction in WKY/SHR rats. Hsp90β inhibition caused the destabilization of upstream mediators in various pathogenic signalling events, thereby effectively ameliorating this nephropathy owing to renal hypoxia and oxidative stress.

scholarly journals Reproductive parameters and oxidative stress status of male rats fed with low and high salt diet

2013 ◽  
Vol 6 (4) ◽  
pp. 267 ◽  
Author(s):  
BolanleO Iranloye ◽  
AyodeleO Morakinyo ◽  
GabrielO Oludare ◽  
LucyC Ekeh ◽  
NaomiA Esume
Keyword(s):  
Oxidative Stress ◽  
High Salt ◽  
Male Rats ◽  
Reproductive Parameters ◽  
High Salt Diet ◽  
Salt Diet ◽  
Oxidative Stress Status ◽  
And Oxidative Stress

scholarly journals Analysis ofHelicobacter pylori cagAPromoter Elements Required for Salt-Induced Upregulation of CagA Expression

2012 ◽  
Vol 80 (9) ◽  
pp. 3094-3106 ◽  
Author(s):  
John T. Loh ◽  
David B. Friedman ◽  
M. Blanca Piazuelo ◽  
Luis E. Bravo ◽  
Keith T. Wilson ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Transcriptional Start Site ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Content Type ◽  
Dna Motif ◽  
Proteomic Approach ◽  
Increased Risk ◽  
H Pylori

ABSTRACTHelicobacter pyloriinfection and consumption of a high-salt diet are each associated with an increased risk for the development of gastric cancer. To investigate potential synergism between these factors, we used a global proteomic approach to analyzeH. pyloristrains cultured in media containing varying salt concentrations. Among the differentially expressed proteins identified, CagA exhibited the greatest increase in expression in response to high salt concentrations. Analysis of 36H. pyloristrains isolated from patients in two regions of Colombia with differing incidences of gastric cancer revealed marked differences among strains in salt-responsive CagA expression. Sequence analysis of thecagApromoter region in these strains revealed a DNA motif (TAATGA) that was present in either one or two copies. Salt-induced upregulation of CagA expression was detected more commonly in strains containing two copies of the TAATGA motif than in strains containing one copy. Mutagenesis experiments confirmed that two copies of the TAATGA motif are required for salt-induced upregulation of CagA expression. In summary, there is considerable heterogeneity amongH. pyloristrains in salt-regulated CagA expression, and these differences are attributable to variation in a specific DNA motif upstream of thecagAtranscriptional start site.

Overload proteinuria is followed by salt-sensitive hypertension caused by renal infiltration of immune cells

2002 ◽  
Vol 283 (5) ◽  
pp. F1132-F1141 ◽  
Author(s):  
Violeta Alvarez ◽  
Yasmir Quiroz ◽  
Mayerly Nava ◽  
Héctor Pons ◽  
Bernardo Rodríguez-Iturbe
Keyword(s):  
Interstitial Nephritis ◽  
Renal Damage ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Malondialdehyde Content ◽  
Induced Hypertension ◽  
Salt Sensitive Hypertension ◽  
And Control ◽  
And Oxidative Stress

Recent evidence suggests that salt-sensitive hypertension develops as a consequence of renal infiltration with immunocompetent cells. We investigated whether proteinuria, which is known to induce interstitial nephritis, causes salt-sensitive hypertension. Female Lewis rats received 2 g of BSA intraperitoneally daily for 2 wk. After protein overload (PO), 6 wk of a high-salt diet induced hypertension [systolic blood pressure (SBP) = 156 ± 11.8 mmHg], whereas rats that remained on a normal-salt diet and control rats (without PO) on a high-salt diet were normotensive. Administration of mycophenolate mofetil (20 mg · kg−1 · day−1) during PO resulted in prevention of proteinuria-related interstitial nephritis, reduction of renal angiotensin II-positive cells and oxidative stress (superoxide-positive cells and renal malondialdehyde content), and resistance to the hypertensive effect of the high-salt diet (SBP = 129 ± 12.2 mmHg). The present studies support the participation of renal inflammatory infiltrate in the pathogenesis of salt-sensitive hypertension and provide a direct link between two risk factors of progressive renal damage: proteinuria and hypertension.

High-salt diet enhances hippocampal oxidative stress and cognitive impairment in mice

2014 ◽  
Vol 114 ◽  
pp. 10-15 ◽  
Author(s):  
Yun-Zi Liu ◽  
Ji-Kuai Chen ◽  
Zhang-Peng Li ◽  
Ting Zhao ◽  
Min Ni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet

Abstract 370: Upregulation of Renal D5 Dopamine Receptor Ameliorates Hypertension in D3 Deficient Mice

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Xiaoyan Wang ◽  
Crisanto S Escano ◽  
Laureano Asico ◽  
John E Jones ◽  
Alan Barte ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Nadph Oxidase ◽  
Protein Expression ◽  
Dopamine Receptors ◽  
Dopamine Receptor ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Deficient Mice

D 3 dopamine receptor (D 3 R) deficient mice have renin-dependent hypertension but the hypertension is mild and is not associated with oxidative stress. In order to determine if any compensatory mechanism in the kidney is involved in the regulation of blood pressure with disruption of D 3 R, we measured the renal protein expression of dopamine receptors in D 3 R homozygous (D 3 -/-) and heterozygous (D 3 +/-) knockout mice and their wild type (D 3 +/+) littermates. D 5 dopamine receptor (D 5 R) (169±23%, reported as % of D 3 +/+, n=5/group) expression was increased but D 4 dopamine receptors protein expression (59±8%) was decreased, while no significant changes were found with D 1 and D 2 dopamine receptors. Immunocytochemistry showed a stronger renal staining of D 5 R but without a change in renal tubule cell distribution in D 3 -/- relative to D 3 +/+ mice. D 5 R abundance was also increased in D 3 +/- (205±30%, n=5/group) relative to D 3 +/+ mice, while D 1 R abundance was similar between D 3 +/- and D 3 +/+ mice. The increase in D 5 R expression was abolished while blood pressure was increased further in D 3 -/- mice fed a high salt diet. Treatment of the D 1 -like (including D 1 and D 5 receptors) antagonist, SCH23390 , increased the blood pressure to a greater extent in anesthetized D 3 -/- mice than in D 3 +/+ mice (n=4/group), suggesting that the upregulation of D 5 R may modulate the hypertension in mice caused by the disruption of D 3 R. Since dopamine inhibits the NADPH oxidase-induced production of reactive oxygen species (ROS) via the D 5 R, we also measured the protein expression of NOXs in the kidney and isoprostane in the urine. No NADPH oxidase subunit was increased in D 3 -/- and D 3 +/- mice relative to D 3 +/+ mice fed a normal or salt high salt diet, and urinary isoprostane excretion was also similar in D 3 -/- and D 3 +/+ mice. Our findings suggest that the upregulation of D 5 R may minimize the hypertension and prevent oxidative stress in D 3 -/- mice.

scholarly journals Synergistic Promoting Effects ofHelicobacter pyloriInfection and High-salt Diet on Gastric Carcinogenesis in Mongolian Gerbils

2002 ◽  
Vol 93 (10) ◽  
pp. 1083-1089 ◽  
Author(s):  
Koji Nozaki ◽  
Nobuyuki Shimizu ◽  
Ken-ichi Inada ◽  
Tetsuya Tsukamoto ◽  
Manami Inoue ◽  
...  
Keyword(s):  
Gastric Carcinogenesis ◽  
High Salt ◽  
Mongolian Gerbils ◽  
High Salt Diet ◽  
Salt Diet
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