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Acta Physiol (Oxf). 2019 Apr 20:e13285. doi: 10.1111/apha.13285. [Epub ahead of print]
Role of the immune system in vascular function and blood pressure control induced by fecal microbiota transplantation in rats.
Toral M1, Robles-Vera I1, de la Visitación N1, Romero M1,2, Sánchez M1,2, Gómez-Guzmán M1, Rodriguez-Nogales A1,2, Yang T3, Jiménez R1,2,4, Algieri F1,2, Gálvez J1,2,5, Raizada MK3, Duarte J1,2,4.
Author information
Abstract
AIM:
High blood pressure (BP) is associated with gut microbiota dysbiosis. The aim of this study was to investigate whether changes in gut microbiota induced by exchanging the gut microbiota between spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) alter the gut-immune system interaction inducing changes in vascular function and BP.
METHODS:
Twenty-week-old recipient WKY and SHR were orally gavaged with donor fecal contents from WKY or SHR. In additional experiments, we used a design to determine whether blockade of B7-dependent costimulation with CTLA4-Ig or blockade of IL-17 with IL-17-neutralizing antibody could prevent hypertension caused by fecal microbiota transplantation (FMT) from SHR to WKY.
RESULTS:
Correlation analyses identified the bacterial abundance of Turicibacter and S24-7_g that, respectively, positively and negatively correlated with systolic BP. FMT from WKY rats to SHR rats reduced basal systolic BP, restored the imbalance between Th17/Treg in mesenteric lymph nodes (MLNs) and aorta, and improved endothelial dysfunction and vascular oxidative status found in SHR transplanted with SHR faeces. FMT from SHR to WKY increased CD80 and CD86 mRNA levels and T cells activation in MLNs, circulating T cells, aortic T cell infiltration, impaired endothelial function and increased basal SBP. These effects were abolished by blockade of B7-dependent costimulation with CTLA4-Ig. IL-17a neutralizing antibody reduced SBP and improved endothelial dysfunction induced by FMT from SHR to WKY.
CONCLUSION:
Gut microbiota is an important factor involved in the control of BP, as a consequence of its effect in T-cell activation in gut immune system and vascular T-cells accumulation. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
Gut dysbiosis; endothelial dysfunction; hypertension; immune cells
Role of the immune system in vascular function and blood pressure control induced by fecal microbiota transplantation in rats.
Toral M1, Robles-Vera I1, de la Visitación N1, Romero M1,2, Sánchez M1,2, Gómez-Guzmán M1, Rodriguez-Nogales A1,2, Yang T3, Jiménez R1,2,4, Algieri F1,2, Gálvez J1,2,5, Raizada MK3, Duarte J1,2,4.
Author information
Abstract
AIM:
High blood pressure (BP) is associated with gut microbiota dysbiosis. The aim of this study was to investigate whether changes in gut microbiota induced by exchanging the gut microbiota between spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) alter the gut-immune system interaction inducing changes in vascular function and BP.
METHODS:
Twenty-week-old recipient WKY and SHR were orally gavaged with donor fecal contents from WKY or SHR. In additional experiments, we used a design to determine whether blockade of B7-dependent costimulation with CTLA4-Ig or blockade of IL-17 with IL-17-neutralizing antibody could prevent hypertension caused by fecal microbiota transplantation (FMT) from SHR to WKY.
RESULTS:
Correlation analyses identified the bacterial abundance of Turicibacter and S24-7_g that, respectively, positively and negatively correlated with systolic BP. FMT from WKY rats to SHR rats reduced basal systolic BP, restored the imbalance between Th17/Treg in mesenteric lymph nodes (MLNs) and aorta, and improved endothelial dysfunction and vascular oxidative status found in SHR transplanted with SHR faeces. FMT from SHR to WKY increased CD80 and CD86 mRNA levels and T cells activation in MLNs, circulating T cells, aortic T cell infiltration, impaired endothelial function and increased basal SBP. These effects were abolished by blockade of B7-dependent costimulation with CTLA4-Ig. IL-17a neutralizing antibody reduced SBP and improved endothelial dysfunction induced by FMT from SHR to WKY.
CONCLUSION:
Gut microbiota is an important factor involved in the control of BP, as a consequence of its effect in T-cell activation in gut immune system and vascular T-cells accumulation. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
Gut dysbiosis; endothelial dysfunction; hypertension; immune cells
