Letter to the Editor
Clara Cells and Injury Post Lung Transplantation: An Evolving Story
Article first published online: 6 MAR 2013
© Copyright 2013 The American Society of Transplantation and the American Society of Transplant Surgeons
American Journal of Transplantation
Volume 13, Issue 5, page 1370, May 2013
How to Cite
Bourdin, A., Mifsud, N. A., Chanez, B., Chanez, P., Snell, G. and Kotsimbos, T. C. (2013), Clara Cells and Injury Post Lung Transplantation: An Evolving Story. American Journal of Transplantation, 13: 1370. doi: 10.1111/ajt.12184
- Issue published online: 26 APR 2013
- Article first published online: 6 MAR 2013
To the Editor:
We read with interest the recently published report from Kelly et al. in the journal . They found that Bronchiolitis Obliterans Syndrome (BOS) post lung transplantation was associated with both a decrease in the number of Clara cell secretory protein (CCSP) positive cells in the small airways and in CCSP protein levels present in the bronchoalveolar lavage (BAL) at the time of BOS diagnosis. These findings confirm our previously published findings early last year in which a longitudinally followed study cohort of 63 lung transplant recipients (LTRs) revealed that CCSP cell and protein signals were not only reduced at the time of BOS but that, as a group, LTRs who later developed BOS tended to have lower BAL CCSP levels as early as 1 month posttransplantation . In addition, the predictive power of CCSP signal loss was even stronger when IL-8 levels in the BAL were used to adjust for the level of inflammation present at each study time point (the likely importance of this was also pointed out by Kelly et al. in their report). Taking our report together with the more recent findings of Kelly et al., it is suggested that there may be several mechanisms at play relating to Clara cell/CCSP signal loss and BOS development including early loss potentially associated with ischemia-reperfusion injury/primary graft dysfunction and alloreactivity associated loss at various time points throughout the life of the lung allograft. The current evidence supports the possibility that CCSP-positive cells in the small airways and secretion of their immunomodulatory product CCSP play a crucial role in healing and repair following lung injury from various causes. In this setting, any genetic polymorphisms that may more generally influence potential CCSP levels for any given level of injury/inflammatory in the airway microenvironment is likely to be highly relevant. In our report, we also described a frequent CCSP polymorphism in the donor [but not in the recipient] that was associated with lower BAL CCSP levels and BOS development. We believe that this second set of descriptive data reported by Kelly et al. provide confirmatory evidence of our initial findings and strongly support further investigative efforts to explore this line of research in both LTR and other acute and chronic lung injury settings.
The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation.