Pulmonary infection defense after lung transplantation: does airway ischemia play a role?

Curr Opin Organ Transplant. 2010 Oct;15(5):568-71. doi: 10.1097/MOT.0b013e32833debd0.


Purpose of review: During a classical lung transplantation procedure, there is no attempt to restore the bronchial circulation, giving rise to ischemia of the mucosa with initial loss of ciliated function. This might compromise the ciliary function and the infection defense mechanisms of the airways.

Recent findings: Although initially the airways are characterized by ischemia (epithelial sloughing), later on, there seems to be a restoration of the ciliary function and up to now, there is no clear evidence that there is an increased risk of infectious episodes due to the lack of bronchial circulation, although this has not extensively been investigated.

Summary: Local pulmonary defense mechanisms after lung transplantation without bronchial revascularization seem to be preserved at least in a stable condition. Whether the loss of bronchial circulation has a negative impact when complications develop (such as bronchiolitis obliterans syndrome) remains speculative.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Anastomosis, Surgical
  • Animals
  • Bronchial Arteries / immunology
  • Bronchial Arteries / physiopathology
  • Bronchial Arteries / surgery*
  • Cilia / pathology
  • Ciliary Motility Disorders / etiology
  • Ciliary Motility Disorders / physiopathology
  • Humans
  • Inflammation Mediators / metabolism
  • Lung / blood supply*
  • Lung / surgery*
  • Lung Transplantation / adverse effects*
  • Pulmonary Circulation*
  • Reperfusion Injury / etiology*
  • Reperfusion Injury / immunology
  • Reperfusion Injury / pathology
  • Reperfusion Injury / physiopathology
  • Respiratory Mucosa / pathology
  • Respiratory Mucosa / physiopathology
  • Respiratory Tract Infections / etiology*
  • Respiratory Tract Infections / immunology
  • Respiratory Tract Infections / pathology
  • Respiratory Tract Infections / physiopathology
  • Risk Factors
  • Treatment Outcome


  • Inflammation Mediators