The Reactivity of the Cardiovascular System and Immunomodulation by Catecholamines in Juvenile Chronic Arthritis

Authors

  • ANNEMIEKE KAVELAARS,

    Corresponding author
    1. Department of Immunology, University Hospital for Children and Youth “Het Wilhelmina Kinderziekenhuis,” Utrecht, the Netherlands
    Search for more papers by this author
  • TEAU de JONG-de VOS van STEENWIJK,

    1. Department of Immunology, University Hospital for Children and Youth “Het Wilhelmina Kinderziekenhuis,” Utrecht, the Netherlands
    Search for more papers by this author
  • WIETSE KUIS,

    1. Department of Immunology, University Hospital for Children and Youth “Het Wilhelmina Kinderziekenhuis,” Utrecht, the Netherlands
    Search for more papers by this author
  • COBI J. HEIJNEN

    1. Department of Immunology, University Hospital for Children and Youth “Het Wilhelmina Kinderziekenhuis,” Utrecht, the Netherlands
    Search for more papers by this author

Additional correspondence information: Telephone: 31-30-2320-377; Fax: 31-30-2320-712; e-mail: a.kavelaars@wkz.azu.nl

Abstract

Abstract: Juvenile chronic arthritis is associated with clinical symptoms indicating that there is a dysregulation of the sympathetic nervous system (SNS). Our data show that patients with juvenile chronic arthritis have an altered function of the SNS associated with increased central noradrenergic outflow, presumably leading to increased vasoconstriction, resulting in a decreased response to an orthostatic stressor. We also investigated the consequences of the altered reactivity of SNS for the reactivity of the immune system to mediators of the sympathetic nervous system and to glucocorticoids. It appeared that leukocytes of these patients have an altered response to catecholamines. Triggering of the β2-adrenergic receptor leads to reduced cAMP responses that are due to the higher rate of cAMP degradation. In addition, catecholamines induce the production of IL-6 by leukocytes of these patients, via triggering of α1-adrenergic receptors. Healthy controls do not express functional α1-adrenergic receptors.

Ancillary