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Vlad C. Sandulache, PhD; J. Brett Chafin, MD; Ha-Sheng Li-Korotky, MD, PhD; Todd D. Otteson, MD; Joseph E. Dohar, MD; Patricia A. Hebda, PhD

Arch Otolaryngol Head Neck Surg. 2007;133(4):365-374.

Objectives  To determine whether (1) inflammatory mediators IL-1β (interleukin 1β) and prostaglandin E₂ (PGE₂) in mucosal secretions correlate with subglottic mucosal injury; and (2) mucosal fibroblasts contribute to PGE₂ production during mucosal healing.

Design  The subglottic mucosa in rabbits was wounded by means of varied carbon dioxide laser power and duration. Subglottic fibroblasts were exposed to IL-1β and assayed for production of PGE₂.

Subjects  Thirty-eight New Zealand white rabbits were used. Fibroblasts from normal and pathologic human subglottic tissues were grown in culture.

Interventions  Subglottic injury was established in 29 rabbits, and 9 rabbits were sham-wounded. Subglottic mucosal secretions were collected at baseline and days 1, 3, 7, 14, and 21 postoperatively and assayed for IL-1β and PGE₂ by enzyme-linked immunosorbent assay. Tissue was analyzed using quantitative polymerase chain reaction. Fibroblast cultures were exposed to IL-1β and analyzed for PGE₂ and its synthetic enzymes.

Results  Subglottic injury was associated with increased levels of IL-1β and PGE₂ in secretions. More extensive mucosal injury resulted in higher PGE₂ levels at earlier times. Levels of IL-1β were maximal after lesser damage. Expression of IL-β and cyclo-oxygenase 2 was elevated after mucosal injury. Fibroblast treatment with IL-1β resulted in translocation of nuclear factor B, up-regulation of PGE₂ synthetic enzymes, and increased production of endogenous PGE₂.

Conclusions  Mucosal injury is associated with up-regulation of inflammatory genes and parallel increases in secretion levels of IL-1β and PGE₂, key mediators of inflammation and healing. Subglottic mucosal fibroblasts are a potential source of inflammatory mediators after injury or other trauma.

Author Affiliations: Department of Pediatric Otolaryngology, Children's Hospital of Pittsburgh (Drs Sandulache, Chafin, Li-Korotky, Otteson, Dohar, and Hebda), Departments of Otolaryngology (Drs Sandulache, Chafin, Li-Korotky, Otteson, Dohar, and Hebda) and Cell Biology and Physiology (Dr Hebda), University of Pittsburgh, Cellular and Molecular Pathology Program (Drs Sandulache and Hebda) University of Pittsburgh School of Medicine, Department of Speech and Communication Disorders, University of Pittsburgh School of Health and Rehabilitation Sciences (Dr Hebda and Dohar), and the McGowan Institute for Regenerative Medicine (Drs Sandulache, Dohar, and Hebda), Pittsburgh, Pa.

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