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

Head Neck. 2012 Sep;34(9):1283-93. doi: 10.1002/hed.21915. Epub 2011 Nov 11.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cell Differentiation
  • Collagen Type I / metabolism*
  • Female
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Myofibroblasts / cytology*
  • Myofibroblasts / metabolism
  • Trachea / metabolism*
  • Trachea / pathology
  • Tracheal Stenosis / metabolism*
  • Tracheal Stenosis / pathology
  • Young Adult

Substances

  • Collagen Type I