Modulation of allergic lung inflammation in mice by the sympathetic nervous system (SNS).

• Grant number: 18/05307-0
• Support Opportunities: Regular Research Grants
• Duration: June 01, 2018 - August 31, 2020
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Alexandre Salgado Basso
• Grantee: Alexandre Salgado Basso
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

The nervous system can interact with the immune system via the sympathetic nervous system (SNS). It has been already described that lymphoid organs are richly innervated by sympathetic fibers, which exert their actions by releasing mainly noradrenaline. The anatomy of the sympathetic innervation in lymphoid organs such as the spleen and lymph nodes suggests that many immune processes, including antigen presentation and, T cell activation and differentiation, may be under direct influence of the mediators released by sympathetic fibers. Indeed, immune cells, including dendritic cells (DCs) and CD4+T cells, express adrenergic receptors, mainly the beta2 adrenergic receptor (B2AR), being able to receive signals coming from the SNS. Studies addressing how the SNS can influence the development of autoimmune diseases such as the experimental autoimmune encephalomyelitis (EAE) showed that, by signaling via B2AR in immune cells, neurotransmitters released by nerves impair the generation of encephalitogenic responses which are dependent of Th1 and Th17 cells. However, much less is known on how the SNS can modulate Th2 mediated responses such as allergic lung inflammation. This project aims at studying the influence of the SNS on the development of allergic lung inflammation and on the generation of Th2 responses in mice. In order to accomplish our aims we propose the utilization of alpha2a/c adrenergic receptor-deficient mice as a model of SNS hyperactivity. (AU)