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      Spinal cord injury-induced immunodeficiency is mediated by a sympathetic-neuroendocrine adrenal reflex

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          Abstract

          Spinal cord injury causes life-threatening infections. The authors report that this is partially mediated by a maladaptive neuroendocrine reflex extending from the spinal cord to the adrenal glands, where it blocks catecholamines while producing immunosuppressive corticosteroids. The effect depends on the spinal injury level, and normalization of hormones production by the adrenals rescues mice from pneumonia.

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          Central nervous system injury-induced immune deficiency syndrome.

          Christian Meisel, Jan Schwab, Konstantin Prass … (2005)
          Infections are a leading cause of morbidity and mortality in patients with acute CNS injury. It has recently become clear that CNS injury significantly increases susceptibility to infection by brain-specific mechanisms: CNS injury induces a disturbance of the normally well balanced interplay between the immune system and the CNS. As a result, CNS injury leads to secondary immunodeficiency - CNS injury-induced immunodepression (CIDS) - and infection. CIDS might serve as a model for the study of the mechanisms and mediators of brain control over immunity. More importantly, understanding CIDS will allow us to work on developing effective therapeutic strategies, with which the outcome after CNS damage by a host of diseases could be improved by eliminating a major determinant of poor recovery.
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            Reciprocal regulation of the neural and innate immune systems.

            Michael Irwin, Steven Cole (2011)
            Innate immune responses are regulated by microorganisms and cell death, as well as by a third class of stress signal from the nervous and endocrine systems. The innate immune system also feeds back, through the production of cytokines, to regulate the function of the central nervous system (CNS), and this has effects on behaviour. These signals provide an extrinsic regulatory circuit that links physiological, social and environmental conditions, as perceived by the CNS, with transcriptional 'decision-making' in leukocytes. CNS-mediated regulation of innate immune responses optimizes total organism fitness and provides new opportunities for therapeutic control of chronic infectious, inflammatory and neuropsychiatric diseases.
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              Adrenergic nerves govern circadian leukocyte recruitment to tissues.

              Christoph Scheiermann, Yuya Kunisaki, Daniel Lucas … (2012)
              The multistep sequence leading to leukocyte migration is thought to be locally regulated at the inflammatory site. Here, we show that broad systemic programs involving long-range signals from the sympathetic nervous system (SNS) delivered by adrenergic nerves regulate rhythmic recruitment of leukocytes in tissues. Constitutive leukocyte adhesion and migration in murine bone marrow (BM) and skeletal-muscle microvasculature fluctuated with circadian peak values at night. Migratory oscillations, altered by experimental jet lag, were implemented by perivascular SNS fibers acting on β-adrenoreceptors expressed on nonhematopoietic cells and leading to tissue-specific, differential circadian oscillations in the expression of endothelial cell adhesion molecules and chemokines. We showed that these rhythms have physiological consequences through alteration of hematopoietic cell recruitment and overall survival in models of septic shock, sickle cell vaso-occlusion, and BM transplantation. These data provide unique insights in the leukocyte adhesion cascade and the potential for time-based therapeutics for transplantation and inflammatory diseases.
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                Author and article information

                Journal
                Title: Nature Neuroscience
                Abbreviated Title: Nat Neurosci
                Publisher: Springer Nature
                ISSN (Print): 1097-6256
                ISSN (Electronic): 1546-1726
                Publication date Created: September 18 2017
                Publication date (Print): September 18 2017
                Volume:
                Issue:
                Article
                DOI: 10.1038/nn.4643
                PubMed ID: 28920935
                SO-VID: 61d3946a-32fd-4fa4-b8b4-8240d3d2d7cf
                Copyright © © 2017
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