Abstract
Iatrogenic laryngotracheal stenosis (LTS) is pathologic airway narrowing due to scar formation following endotracheal intubation or tracheostomy. It is a chronic and recurrent disease that results in significant morbidity or even mortality. Current data suggests that inflammatory pathways play a significant role in mediating the deposition of collagen and extracellular matrix to generate this scar. In particular, the T-helper 2 cell and M2 macrophage axis appears to be activated in both animal models and patients with iatrogenic LTS. Interleukin-6 production in response to hypoxia has also been implicated. In this paper, we review the data supporting the roles of various inflammatory pathways in the pathogenesis of iatrogenic LTS, discuss potential therapeutic approaches targeting these mechanisms, and outline areas for future study.
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