Abstract
The autonomic nervous system (ANS) and the immune system are deeply interrelated. The ANS regulates both innate and adaptive immunity through the sympathetic and parasympathetic branches, and an imbalance in this system can determine an altered inflammatory response as typically observed in chronic conditions such as systemic autoimmune diseases. Rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis all show a dysfunction of the ANS that is mutually related to the increase in inflammation and cardiovascular risk. Moreover, an interaction between ANS and the gut microbiota has direct effects on inflammation homeostasis. Recently vagal stimulation techniques have emerged as an unprecedented possibility to reduce ANS dysfunction, especially in chronic diseases characterized by pain and a decreased quality of life as well as in chronic inflammation.
Highlights
The autonomic nervous system (ANS) has two main components, the sympathetic and the parasympathetic branches, that dynamically regulate the visceral functions [1]
In a recent study on a rabbit model of postural orthostatic tachycardia syndrome (POTS) induced by M2 muscarinic acetylcholine receptor-activating autoantibodies immunization, transcutaneous vagus nerve stimulation contributes to increasing acetylcholine with consequent reduction in both inflammation and cardiovagal dysfunction [75]
Most of the studies report a reduction in cardiac parasympathetic activity (n = 20/26 studies, prevalence 77%) assessed through a reduced heart rate variability (HRV), that is a noninvasive method to investigate the status of cardiovascular autonomic control, and a high Resting Heart Rate (RHR) [113]
Summary
The autonomic nervous system (ANS) has two main components, the sympathetic and the parasympathetic branches, that dynamically regulate the visceral functions [1]. Since ANS can regulate inflammation in chronic and acute conditions, autonomic dysfunction can have a pivotal influence on the onset and progression of many diseases where the immune response is involved, such as autoimmune diseases [2,3,4]. Given these premises, in the present review we will explore the interaction between immunity and ANS, focusing on the mutual contribution with both the innate and the adaptive immunity. We will explore from a more clinical point of view, what is currently known about ANS in three systemic autoimmune diseases in which immunity and inflammation are the main pathological processes such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and systemic sclerosis (SSc)
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