Autonomic nervous system and inflammation

      Trauma leading to tissue injury, invasion of microbes and infection activates the inflammatory pathway that consists of inducers, sensors, mediators and effectors of inflammation (
      • Medzhitov R.
      Origin and physiological roles of inflammation.
      ,
      • Medzhitov R.
      Inflammation 2010: new adventures of an old flame.
      ). Broken cells, microbes and their products and neuropeptides released by terminals of nociceptive primary afferent neurons are sensed by sentinel cells located in the injured tissue such as mast cells, macrophages and dendritic cells. These cells release many substances that turn on and mediate the “molecular machinery” of the immune system and activate several other effectors, such as endothelial cells and vascular smooth muscle cells resulting in the full development of inflammation. This inflammatory process involves the recruitment of different groups of immune cells such as neutrophils, antigen-presenting cells and lymphocytes releasing a host of substances that amplify inflammation and vascular endothelia, platelets and coagulation factors. The inflammatory response needs to develop as quickly as possible to terminate the spread of infection, to limit further tissue injury and to protect the host. This process is organized by a molecular program that actively coordinates the action and interaction of the different cellular components that are geared in their intensity by the input signals produced by the tissue injury and the invading microbes. This initial fast developing inflammatory reaction resolves quickly once the tissue has been cleared of microbes and their toxins and of other detrimental consequences of the injury following cell necrosis. The resolution of the inflammation is also an active process orchestrated by a molecular working program that involves more or less the same cells of the immune system and associated cells. The development and resolution of inflammation are finely tuned to each other according to the size of tissue injury to avoid a too early resolution of inflammation and subsequent expansion of microbes and their toxins in the body on one side and to prevent an uncontrolled prolongation of inflammation developing into chronic inflammation on the other (
      • Nathan C.
      Points of control in inflammation.
      ,
      • Serhan C.N.
      • Savill J.
      Resolution of inflammation: the beginning programs the end.
      ,
      • Medzhitov R.
      Origin and physiological roles of inflammation.
      ,
      • Nathan C.
      • Ding A.
      Nonresolving inflammation.
      ).

      Keywords

      To read this article in full you will need to make a payment

      References

      1. Ader A. Fourth edition. Psychoneuroimmunology. volume 1 and 2. Academic Press Elsevier, Amsterdam2007
        • Jänig W.
        The Integrative Action of the Autonomic Nervous System: Neurobiology of Homeostasis.
        Cambridge University Press, Cambridge, New York, 2006
      2. King H.H. Jänig W. Patterson M.H. The Science and Clinical Application of Manual Therapy. Churchill Livingstone Elsevier, Edinburgh2011
        • Martelli D.
        • Yao S.T.
        • McKinley M.J.
        • McAllen R.M.
        Reflex control of inflammation by sympathetic nerves, not the vagus.
        J. Physiol. 2014; (in press)
      3. Mathias C.J. Bannister R. Autonomic Failure. Fifth edition. Oxford University Press, New York Oxford2013
      4. Mayer E.M. Bushnell M.C. Functional Pain Syndromes: Presentation and Pathophysiology. IASP Press, Seattle2009
        • Medzhitov R.
        Origin and physiological roles of inflammation.
        Nature. 2008; 454: 428-435
        • Medzhitov R.
        Inflammation 2010: new adventures of an old flame.
        Cell. 2010; 140: 771-776
        • Nance D.M.
        • Sanders V.M.
        Autonomic innervation and regulation of the immune system (1987–2007).
        Brain Behav. Immun. 2007; 21: 736-745
        • Nathan C.
        Points of control in inflammation.
        Nature. 2002; 420: 846-852
        • Nathan C.
        • Ding A.
        Nonresolving inflammation.
        Cell. 2010; 140: 871-882
        • Serhan C.N.
        • Savill J.
        Resolution of inflammation: the beginning programs the end.
        Nat. Immunol. 2005; 6: 1191-1197