title: Effects of raised-intensity phonation on inflammatory mediator gene expression in normal rabbit vocal fold.
abstract: OBJECTIVE
  To investigate the hypothesis that a transient episode of raised-intensity phonation causes a significant increase in vocal fold inflammatory messenger RNA (mRNA) expression in vivo.
  
  
  METHODS
  Prospective animal study.
  
  
  METHODS
  Laboratory.
  
  
  METHODS
  Ten New Zealand White breeder rabbits received 30 minutes of experimentally induced modal or raised-intensity phonation, followed by a 30-minute recovery period. A separate group of five rabbits served as sham controls. Real-time polymerase chain reaction was performed to investigate the mRNA expression of interleukin 1beta (IL-1beta), transforming growth factor beta-1 (TGFbeta1), and cyclooxygenase-2 (COX-2). Separate one-way analysis of variance (ANOVA) tests were used to investigate differences in gene expression across groups, with an appropriate alpha correction of 0.016 to control for type I error. Significant main effects were further examined using Fisher's least significant difference.
  
  
  RESULTS
  ANOVA revealed that there were differences for IL-1beta, TGFbeta1, and COX-2 between sham control, modal phonation, and raised-intensity phonation (P 0.0001). Pairwise comparisons revealed that the expression of IL-1beta, COX-2, and TGFbeta1 increased significantly during raised-intensity phonation, compared to modal phonation and sham control (P 0.0001).
  
  
  CONCLUSIONS
  Results provided support for the hypothesis that a transient episode of raised-intensity phonation causes a significant increase in vocal fold inflammatory mRNA expression. Future studies will investigate the signal transduction pathways and mechanisms regulating the vocal fold inflammatory response. The long-term goal of these studies is to advance understanding of the molecular and cellular events underlying phonation-related tissue alterations.
authors.affiliation: Department of Otolaryngology, Vanderbilt University Bill Wilkerson Center for Otolaryngology and Communication Sciences, Nashville, TN, USA.
authors.forename: Erik R
authors.initials: ER
authors.lastname: Swanson
authors.forename: Tsunehisa
authors.initials: T
authors.lastname: Ohno
authors.forename: Dave
authors.initials: D
authors.lastname: Abdollahian
authors.forename: C Gaelyn
authors.initials: CG
authors.lastname: Garrett
authors.forename: Bernard
authors.initials: B
authors.lastname: Rousseau
mesh_terms: D000818:Animals; D051546:Cyclooxygenase 2 / Q000235:genetics* / Q000378:metabolism; D015870:Gene Expression; D053583:Interleukin-1beta / Q000235:genetics* / Q000378:metabolism; D010699:Phonation / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011817:Rabbits; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053773:Transforming Growth Factor beta1 / Q000235:genetics* / Q000378:metabolism; D014827:Vocal Cords / Q000378:metabolism* / Q000502:physiology
chemical_list: D053583:Interleukin-1beta; D012333:RNA, Messenger; D053773:Transforming Growth Factor beta1; D051546:Cyclooxygenase 2