title: Modulation of inflammatory and profibrotic signaling in a rabbit model of acute phonotrauma using triamcinolone.
abstract: OBJECTIVE
  To investigate the hypothesis that prophylactic triamcinolone modulates acute vocal fold inflammatory and profibrotic signaling during acute phonotrauma.
  
  
  METHODS
  In vivo rabbit phonation model.
  
  
  METHODS
  Academic medical center.
  
  
  METHODS
  Forty New Zealand white breeder rabbits were randomly assigned to 1 of 4 groups: control (no intervention), no treatment (30 minutes of raised intensity phonation), sham treatment (bilateral intralaryngeal triamcinolone acetonide injection at 0 µg/25 µL followed by 30 minutes of raised intensity phonation), or steroid treatment (bilateral intralaryngeal triamcinolone acetonide injection at 400 µg/25 µL followed by 30 minutes of raised intensity phonation). Quantitative polymerase chain reaction (qPCR) was used to investigate gene expression levels of cyclooxygenase-2 (COX-2), interleukin (IL)-1β, and transforming growth factor (TGF)-β1.
  
  
  RESULTS
  Results revealed a significant main effect for COX-2 (P = .002). Post hoc testing revealed that rabbits receiving no treatment (15.10) had higher COX-2 gene expression than control (5.90; P < .001). There were no significant differences in COX-2 expression between treatment groups. Results revealed a significant main effect for IL-1β (P < .001). Post hoc testing revealed that rabbits receiving no treatment (14.70) had higher IL-1β gene expression than control (6.30) (P = .001). There were no significant differences in IL-1β gene expression between treatment groups. There were no significant differences in TGF-β1 gene expression (P = .525) between treatment and control groups.
  
  
  CONCLUSIONS
  Given conflicting evidence, further studies are necessary to investigate vocal fold steroid injections prior to and following the induction of phonotrauma. Prophylactic administration of triamcinolone immediately prior to acute phonotrauma resulted in no significant changes in COX-2, IL-1β, and TGF-β1 gene transcript levels.
authors.affiliation: Department of Otolaryngology-Head & Neck Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232-8605, USA. joseph.e.hall@vanderbilt.edu
authors.forename: Joseph E
authors.initials: JE
authors.lastname: Hall
authors.forename: Atsushi
authors.initials: A
authors.lastname: Suehiro
authors.forename: Ryan C
authors.initials: RC
authors.lastname: Branski
authors.forename: C Gaelyn
authors.initials: CG
authors.lastname: Garrett
authors.forename: Bernard
authors.initials: B
authors.lastname: Rousseau
mesh_terms: D000208:Acute Disease; D000818:Animals; D051546:Cyclooxygenase 2 / Q000187:drug effects / Q000235:genetics; D004195:Disease Models, Animal; D005355:Fibrosis / Q000235:genetics / Q000517:prevention & control; D015870:Gene Expression / Q000187:drug effects; D005938:Glucocorticoids / Q000627:therapeutic use*; D007249:Inflammation / Q000235:genetics / Q000517:prevention & control; D053583:Interleukin-1beta / Q000187:drug effects / Q000235:genetics*; D011817:Rabbits; D015398:Signal Transduction; D053773:Transforming Growth Factor beta1 / Q000187:drug effects / Q000235:genetics; D014221:Triamcinolone / Q000627:therapeutic use*; D014827:Vocal Cords / Q000473:pathology*; D014832:Voice Disorders / Q000517:prevention & control*
chemical_list: D005938:Glucocorticoids; D053583:Interleukin-1beta; D053773:Transforming Growth Factor beta1; D014221:Triamcinolone; D051546:Cyclooxygenase 2