Myofibroblast persistence and collagen type I accumulation in the human stenotic trachea.

Abstract

Postintubation tracheal stenosis (PITS) is associated with an increased use of assisted ventilation in intensive care units. We investigated both collagen type I accumulation and myofibroblast localization in human PITS lesions excised for surgical therapeutic procedures, compared with normal tracheas. We analyzed 2 segments of normal tracheas and 10 segments of PITS that were stained by hematoxylin-eosin and picrosirius red techniques and processed for immunohistochemistry using antibodies against both α-smooth muscle actin (α-sma) for myofibroblast detection, and collagen type I. We showed a significant increase in collagen deposition in PITS specimens compared with normal tracheas. We found spindle-shaped α-sma-positive cells (myofibroblasts) in the subepithelial layer of all pathologic tracheas, and the persistence of an intense myofibroblast network at PITS sites. Tracheal wall thickening in PITS is due to a deranged collagen remodeling that is related to myofibroblast activation.