title: Burn-induced organ dysfunction: vagus nerve stimulation attenuates organ and serum cytokine levels.
abstract: BACKGROUND
  The interaction of the CNS and the immune system is well known. A parasympathetic anti-inflammatory pathway has recently been described. Both electrical and pharmacological parasympathetic stimulation attenuate proinflammatory mediator generation. Burn induces abacterial cytokine generation and we sought to evaluate whether parasympathetic stimulation after experimental burn decreases cardiodepressive mediator generation.
  
  
  METHODS
  A 30% TBSA full-thickness rat burn model was used. After microsurgical preparation of the cervical portion of the vagus nerve, we performed electric vagus nerve stimulation. Serum was harvested and organ samples of heart and liver were homogenized. Samples were subjected to sandwich-ELISA specific for TNF-alpha, IL-1beta and IL-6. Heart rate measurements were done using left ventricular microcatheterization. Statistical analysis was done using Student's t-tests and analysis of variance (ANOVA).
  
  
  RESULTS
  Burn induced a significant rise of TNF-alpha, IL-1beta and IL-6 in organ homogenates and serum. After cervical vagal electrostimulation, serum and organ homogenate levels of proinflammatory cytokines were markedly reduced compared to burn controls. Left ventricular microcatheter assessment demonstrated no cardiodepressive effect of the vagal stimulation itself.
  
  
  CONCLUSIONS
  Our results encourage further research regarding the neuroimmunologic background of burn, possibly leading to the development of a novel therapeutic approach to burn-induced organ dysfunction and immunodysregulation.
authors.affiliation: Department of Plastic, Hand and Reconstructive Surgery, Burn Center, Medizinische Hochschule Hannover, Germany. niederbichler.andreas@mh-hannover.de
authors.forename: Andreas D
authors.initials: AD
authors.lastname: Niederbichler
authors.forename: Stephan
authors.initials: S
authors.lastname: Papst
authors.forename: Leif
authors.initials: L
authors.lastname: Claassen
authors.forename: Andreas
authors.initials: A
authors.lastname: Jokuszies
authors.forename: Lars
authors.initials: L
authors.lastname: Steinstraesser
authors.forename: Tobias
authors.initials: T
authors.lastname: Hirsch
authors.forename: Mehmet A
authors.initials: MA
authors.lastname: Altintas
authors.forename: Kyros R
authors.initials: KR
authors.lastname: Ipaktchi
authors.forename: Kerstin
authors.initials: K
authors.lastname: Reimers
authors.forename: Theresia
authors.initials: T
authors.lastname: Kraft
authors.forename: Peter M
authors.initials: PM
authors.lastname: Vogt
mesh_terms: D000818:Animals; D002056:Burns / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy; D016207:Cytokines / Q000097:blood / Q000378:metabolism*; D006339:Heart Rate; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism; D053583:Interleukin-1beta / Q000097:blood / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D008099:Liver / Q000276:immunology; D008297:Male; D009206:Myocardium / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000378:metabolism; D055536:Vagus Nerve Stimulation / Q000379:methods*
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha