Are the innate and adaptive immune systems setting hypertension on fire?

Author(s)

Bomfim, Gisele F. ; Rodrigues, Fernanda Luciano ; Carneiro, Fernando S.

• Document type: Review article
• Source: PHARMACOLOGICAL RESEARCH; v. 117, p. 377-393, MAR 2017.
• Web of Science Citations: 14

Abstract

Hypertension is the most common chronic cardiovascular disease and is associated with several pathological states, being an important cause of morbidity and mortality around the world. Low-grade inflammation plays a key role in hypertension and the innate and adaptive immune systems seem to contribute to hypertension development and maintenance. Hypertension is associated with vascular inflammation, increased vascular cytokines levels and infiltration of immune cells in the vasculature, kidneys and heart. However, the mechanisms that trigger inflammation and immune system activation in hypertension are completely unknown. Cells from the innate immune system express pattern recognition receptors (PRR), which detect conserved pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPS) that induce innate effector mechanisms to produce endogenous signals, such as inflammatory cytokines and chemokines, to alert the host about danger. Additionally, antigen-presenting cells (APC) act as sentinels that are activated by PAMPs and DAMPs to sense the presence of the antigen/neoantigen, which ensues the adaptive immune system activation. In this context, different lymphocyte types are activated and contribute to inflammation and end-organ damage in hypertension. This review will focus on experimental and clinical evidence demonstrating the contribution of the innate and adaptive immune systems to the development of hypertension. (C) 2017 Elsevier Ltd. All rights reserved. (AU)

• FAPESP's process: 15/21976-1 - Cardiovascular autonomic control in toll-like receptor 9 knockout mice with hypertension induced by angiotensin II.
• Grantee: Fernanda Luciano Rodrigues
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• FAPESP's process: 10/17362-4 - Mechanisms of erectile dysfunction on heart failure
• Grantee: Fernando Silva Carneiro
• Support Opportunities: Research Grants - Young Investigators Grants
• FAPESP's process: 16/11988-5 - NLRP3 contribution to the pro-inflammatory effect of ET-1 in corpora cavernosa smooth muscle cells: relevance in erectile function.
• Grantee: Fernando Silva Carneiro
• Support Opportunities: Regular Research Grants