Open AccessEffects of raised‐intensity phonation on inflammatory mediator gene expression in normal rabbit vocal fold
Author(s) -
Swanson Erik R.,
Ohno Tsunehisa,
Abdollahian Dave,
Garrett C. Gaelyn,
Rousseau Bernard
Publication year - 2010
Publication title -
otolaryngology–head and neck surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.232
H-Index - 121
eISSN - 1097-6817
pISSN - 0194-5998
DOI - 10.1016/j.otohns.2010.04.264
Subject(s) - phonation , analysis of variance , medicine , audiology
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. STUDY DESIGN Prospective animal study. SETTING Laboratory. SUBJECTS AND 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 1β (IL‐1β), transforming growth factor β (TGFβ1), 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‐1β, TGFβ1, and COX‐2 between sham control, modal phonation, and raised‐intensity phonation ( P < 0.0001). Pairwise comparisons revealed that the expression of IL‐1β, COX‐2, and TGFβ1 increased significantly during raised‐intensity phonation, compared to modal phonation and sham control ( P < 0.0001). CONCLUSION: 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.