Autonomic nervous system and neuroimmune interactions: New insights and clinical implications

Normal organ function, homeostasis, and adaptation through change (allostasis) require close reciprocal interactions between the autonomic and the immune systems. The 3 subdivisions of the autonomic nervous system—sympathetic, parasympathetic, and enteric nervous system (ENS)—as well as primary sensory afferents, receive signals from immune cells and release neurochemical transmitters that regulate the functions of these cells. These neuroimmune interactions occur at multiple levels, including the gut, the CNS, and lymphoid organs. For example, enteric neurons and glial cells interact with enteroendocrine cells and local macrophages and can sense signals from the gut lumen, including those from the microbiota; these signals elicit local immune responses and reach the CNS via humoral and neural pathways. Interleukins (ILs) and other signals from immune cells can access the hypothalamus via the neurovascular unit or circumventricular organs; these signals can also activate receptors in nerve terminals, such as vagal afferents, and thereby reach the brainstem. In response to these signals, the CNS initiates immunomodulatory autonomic and endocrine responses. For example, sympathetic output to lymphoid organs, including the spleen, elicits potent anti-inflammatory responses via β2 adrenergic receptors (adrenoceptors) expressed in multiple cells of the innate and adaptive immune systems. Vagal efferents affect immune responses in the gut via the ENS, and both vagal and dorsal root ganglion afferents trigger immunomodulatory responses via antidromic release of neuropeptides and other signals at the target organs. Since the last review on autonomic control of immune function in this series,1 studies performed primarily on mice have provided new insight into the role of the microbiota, enteric neurons and glial cells, and autonomic immunomodulatory pathways in these neuroimmune interactions. These studies have elucidated some mechanisms by which these interactions may contribute to the pathophysiology of neurologic disorders including multiple sclerosis (MS) and spinal cord injury (SCI). These findings thus have potential therapeutic implications. There are several recent reviews on these topics.2–12

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