Salt, inflammation, IL-17 and hypertension

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Salt, inflammation, IL-17 and hypertension. / Wenzel, Ulrich O; Bode, Marlies; Kurts, Christian; Ehmke, Heimo.

in: BRIT J PHARMACOL, Jahrgang 176, Nr. 12, 06.2019, S. 1853-1863.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ReviewForschung

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Wenzel, UO, Bode, M, Kurts, C & Ehmke, H 2019, 'Salt, inflammation, IL-17 and hypertension', BRIT J PHARMACOL, Jg. 176, Nr. 12, S. 1853-1863. https://doi.org/10.1111/bph.14359

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Bibtex

@article{4f55c0c01f4e44079c15573dcbc6cddb,
title = "Salt, inflammation, IL-17 and hypertension",
abstract = "Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to haemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign microorganisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Over the past few years, important findings have revolutionized hypertension research. Firstly, in 2007, a seminal paper showed that adaptive immunity is involved in the pathogenesis of hypertension. Secondly, salt storage in the skin and its consequences for cardiovascular physiology were discovered. Thirdly, after the discovery that salt promotes the differentiation of CD4+ T cells into TH 17 cells, it was demonstrated that salt directly changes several cells of the innate and adaptive immune system and aggravates autoimmune disease but may improve antimicrobial defence. Herein, we will review pathways of activation of immune cells by salt in hypertension as the framework for understanding the multiple roles of salt and immunity in arterial hypertension and autoimmune disease. LINKED ARTICLES: This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc.",
keywords = "Journal Article, Review",
author = "Wenzel, {Ulrich O} and Marlies Bode and Christian Kurts and Heimo Ehmke",
note = "{\textcopyright} 2018 The British Pharmacological Society.",
year = "2019",
month = jun,
doi = "10.1111/bph.14359",
language = "English",
volume = "176",
pages = "1853--1863",
journal = "BRIT J PHARMACOL",
issn = "0007-1188",
publisher = "Wiley-Blackwell",
number = "12",

}

RIS

TY - JOUR

T1 - Salt, inflammation, IL-17 and hypertension

AU - Wenzel, Ulrich O

AU - Bode, Marlies

AU - Kurts, Christian

AU - Ehmke, Heimo

N1 - © 2018 The British Pharmacological Society.

PY - 2019/6

Y1 - 2019/6

N2 - Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to haemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign microorganisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Over the past few years, important findings have revolutionized hypertension research. Firstly, in 2007, a seminal paper showed that adaptive immunity is involved in the pathogenesis of hypertension. Secondly, salt storage in the skin and its consequences for cardiovascular physiology were discovered. Thirdly, after the discovery that salt promotes the differentiation of CD4+ T cells into TH 17 cells, it was demonstrated that salt directly changes several cells of the innate and adaptive immune system and aggravates autoimmune disease but may improve antimicrobial defence. Herein, we will review pathways of activation of immune cells by salt in hypertension as the framework for understanding the multiple roles of salt and immunity in arterial hypertension and autoimmune disease. LINKED ARTICLES: This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc.

AB - Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to haemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign microorganisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Over the past few years, important findings have revolutionized hypertension research. Firstly, in 2007, a seminal paper showed that adaptive immunity is involved in the pathogenesis of hypertension. Secondly, salt storage in the skin and its consequences for cardiovascular physiology were discovered. Thirdly, after the discovery that salt promotes the differentiation of CD4+ T cells into TH 17 cells, it was demonstrated that salt directly changes several cells of the innate and adaptive immune system and aggravates autoimmune disease but may improve antimicrobial defence. Herein, we will review pathways of activation of immune cells by salt in hypertension as the framework for understanding the multiple roles of salt and immunity in arterial hypertension and autoimmune disease. LINKED ARTICLES: This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc.

KW - Journal Article

KW - Review

U2 - 10.1111/bph.14359

DO - 10.1111/bph.14359

M3 - SCORING: Review article

C2 - 29767465

VL - 176

SP - 1853

EP - 1863

JO - BRIT J PHARMACOL

JF - BRIT J PHARMACOL

SN - 0007-1188

IS - 12

ER -