Modulation of inflammatory and profibrotic signaling in a rabbit model of acute phonotrauma using triamcinolone.

Abstract

To investigate the hypothesis that prophylactic triamcinolone modulates acute vocal fold inflammatory and profibrotic signaling during acute phonotrauma. In vivo rabbit phonation model. Academic medical center. 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 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. 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.