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

BACKGROUND 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. METHODS 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. RESULTS 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. CONCLUSIONS Tracheal wall thickening in PITS is due to a deranged collagen remodeling that is related to myofibroblast activation.