| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 2006;82:1050-1051
© 2006 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery, Room Ee 173, Erasmus MC Rotterdam, Dr. Molewaterplein 50, Rotterdam, 3015 GE The Netherlands
(Email: npvdkaaij{at}gmail.com; a.j.j.c.bogers{at}erasmusmc.nl).
The outcome after human lung transplantation remains limited, mainly due to development of the bronchiolitis obliterans syndrome (BOS). Development of BOS may be considered as a multiple injury hit model, in which all lung injury-causing factors (eg, ischemia-reperfusion injury, pneumonia, rejection, donor ventilation, and cytomegalovirus [CMV]) seem to have a (major or minor) role in BOS development. All these factors may interplay in BOS initiation and progression. However, pathological pathways by which (acute) lung injury factors may contribute to and interplay in BOS development and progression are mostly unclear.
The hypothesis of the experimental study by Kuo and colleagues [1] was to determine whether a relation between respiratory virus infection and chronic rejection exists. The authors clearly demonstrated enhanced allograft rejection after viral infection in a mouse tracheal transplant model. Nevertheless, in a clinical setting, several studies have investigated the effect of respiratory viruses on the outcome of human lung transplantation. In this regard, Kumar and colleagues [2] have shown that community acquired respiratory viruses (CARV) are associated with the development of acute rejection and BOS. In previous reports from Kuo's group, it was proven that CARV infections are linked to an increased risk of BOS development, BOS progression, and death, independent of other risk factors like acute rejection [3, 4]. Furthermore, Billings and colleagues [5] have found a link between lower respiratory tract infections and high grade BOS development and other clinical studies have also demonstrated a correlation between CMV and BOS [6]. However, some clinical studies could not confirm an association between CMV infection and BOS. Nevertheless, a fall in CMV incidence after the introduction of ganciclovir prophylaxis resulted in reduced incidence of BOS [7]. Moreover, ganciclovir resistance causes earlier BOS onset [8]. Finally in a study by Westall and colleagues [9], a strong association between BOS and early human cytomegalovirus DNAaemia was demonstrated.
In an experimental setting of chronic airway rejection, viral and bacterial infection resulted in enhanced development of chronic airway and vascular rejection in a rat lung transplantation model [10]. Moreover, a synergistic role between viral infections and chronic rejection in the development of BOS has been shown before in an experimental lung transplantation study by Winter and colleagues [11].
With the aforementioned literature in mind, this well-executed study by Kuo and associates [1] provides us with an experimental model rather than new insights in the contribution of respiratory viruses to human BOS development, since several experimental and clinical studies already suggested a relation. The challenge is to use this model and the experimental setting to study underlying pathologic mechanisms by which these factors may contribute and interplay in BOS development. In our opinion, the question whether respiratory viruses are a risk factor for BOS development should be answered affirmatively and studied quantitatively at a clinical level of human lung transplantation, whereas the laboratory could be better used to unravel underlying pathways and investigate treatment modalities of BOS onset and progression.
 |
References |
|---|
 Top References |
|---|
Related Article
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
