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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Sympathetic activation triggers systemic interleukin-10 release in immunodepression induced by brain injury.

The mechanism of immunodepression after brain injury is not yet clear. Here we demonstrate rapid systemic release of the immunoinhibitory cytokine interleukin-10, monocytic deactivation and a high incidence of infection in patients with 'sympathetic storm' due to acute accidental or iatrogenic brain trauma. In vitro studies showed that within minutes catecholamines trigger the secretion of interleukin-10 from unstimulated monocytes through a beta-adrenoreceptor-mediated, cAMP/protein kinase A-dependent pathway. We found that in a rat model of acute brain injury, the beta-receptor antagonist propranolol prevented the increase of interleukin-10 plasma levels. Rapid monocytic interleukin-10 release after sympathetic activation may represent a common pathway for immunodepression induced by stress and injury.[1]

References

  1. Sympathetic activation triggers systemic interleukin-10 release in immunodepression induced by brain injury. Woiciechowsky, C., Asadullah, K., Nestler, D., Eberhardt, B., Platzer, C., Schöning, B., Glöckner, F., Lanksch, W.R., Volk, H.D., Döcke, W.D. Nat. Med. (1998) [Pubmed]
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