## Objectives: Vocal fold injury can be irreversible, leading to vocal fold scarring, with permanent functional effects and no optimal treatment. a porcine model of vocal fold scarring was used to test effects of decorin and primed vocal fold fibroblasts in vitro using a cell migration assay and im
The effects of cigarette smoke condensate on vocal fold transepithelial resistance and inflammatory signaling in vocal fold fibroblasts
✍ Scribed by Ryan C. Branski; Hang Zhou; Dennis H. Kraus; Mahalakshmi Sivasankar
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 264 KB
- Volume
- 121
- Category
- Article
- ISSN
- 0023-852X
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Objectives/Hypothesis:
In response to chronic cigarette smoke exposure, a subset of patients present with edematous vocal folds, characteristically referred to as Reinke's edema. This phenotype differs from the tissue changes associated with prolonged smoke exposure in the lower airway, and the mechanism underlying Reinke's edema remains poorly described. We hypothesize that the effects of smoke are diffuse and involve both the epithelium and mucosa.
Study Design:
In vitro, ex vivo experiment.
Methods:
Transepithelial resistance (R~T~) was quantified in an ex vivo, viable, porcine vocal fold model. Excised tissue was exposed to cigarette smoke condensate (CSC) and R~T~ was computed at baseline and 1 and 4 hours after exposure. In vitro, human vocal fold fibroblasts were exposed to CSC. Cyclooxygenase 2 (COX‐2), microsomal prostaglandin E synthase‐1, and 15‐hydroxyprostaglandin dehydrogenase mRNA expression were assessed at 4 hours. Prostaglandin E2 (PGE2) synthesis was quantified via immunoassay following 24 hours of CSC exposure.
Results:
CSC had no effect on R~T~. CSC did, however, induce COX‐2 mRNA expression as well as its downstream lipid mediator PGE2. PGE2 metabolism appears to be regulated via both synthetic and degradative enzymes in response to cigarette smoke.
Conclusions:
In vitro, CSC initiates an inflammatory response in vocal fold fibroblasts. However, in isolation, the epithelial resistance is not altered by CSC, at least acutely. These data may suggest a role for the interaction between the inflammatory response in the mucosa and compromised epithelial barrier function, as has been shown in other tissues. Laryngoscope, 2011
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