This study was supported by Fundação para a Ciéncia e Tecnologia (FCT) Project No. POCTI/NSE/46399/2002, FEDER, and Fundação Calouste Gulbenkian Project No. 74551.
A New Model of Laryngitis: Neuropeptide, Cyclooxygenase, and Cytokine Profile†
Version of Record online: 2 JAN 2009
Copyright © 2008 The Triological Society
Volume 118, Issue 1, pages 78–86, January 2008
How to Cite
Lima-Rodrigues, M., Valle-Fernandes, A., Lamas, N., Cruz, A., Baltazar, F., Milanezi, F., Nunes, R., Reis, R. M., Pedrosa, J., Castro, A. G. and Almeida, A. (2008), A New Model of Laryngitis: Neuropeptide, Cyclooxygenase, and Cytokine Profile. The Laryngoscope, 118: 78–86. doi: 10.1097/MLG.0b013e3181492400
- Issue online: 2 JAN 2009
- Version of Record online: 2 JAN 2009
- Manuscript Accepted: 27 JUL 2007
- Laryngeal inflammation;
- nasogastric intubation;
- mRNA expression;
- reverse-transcriptase polymerase chain reaction analysis;
- animal model
Objectives/Hypothesis: To develop and characterize a new model of laryngeal inflammation by analyzing the presence of neurogenic peptides and expression of cyclooxygenases (COX) and cytokines in the mucosa.
Study Design: Laryngitis induced by nasogastric intubation (NGI) was evaluated by histopathologic changes of the mucosa, alterations in calcitonin gene related peptide (CGRP) and substance P (SP) neuropeptides in sensory fibers, and COX-1,2, and cytokine (interleukin [IL]-1, IL-6, IL-10, tumor necrosis factor [TNF]-α) expression in the laryngeal mucosa.
Methods: Rats submitted to NGI for 1 to 5 weeks were compared with controls. Laryngeal sections were immunostained for stereologic analysis of SP and CGRP fiber density and number of mucosal cells expressing COX-2. Alterations in inflammatory mediators were evaluated by quantitative reverse-transcriptase polymerase chain reaction.
Results: NGI induced metaplasia of the epithelium and narrowing of the laryngeal lumen because of hypertrophy of laryngeal glandules and edema. An initial decrease in CGRP- and SP-immunoreactive fibers in the laryngeal mucosa (1–3 wk) was reverted with time (5 wk). COX-2 expression in mucosal cells increased progressively, reaching a maximum level at 5 weeks, and was observed in mononuclear immune cells, which is indicative of a chronic inflammatory process. In regard to mRNA expression levels of inflammatory mediators, TNF-α was increased during the 5 week NGI, and IL-10 decreased during the 5 weeks,whereas IL-1β, IL-6, and COX-2 increased in the first 1 to 2 weeks and returned to baseline at 5 weeks.
Conclusions: This NGI model results in laryngeal chronic inflammation without direct mechanical aggression of the mucosa and may contribute to the study of future therapeutic approaches to this pathology.