Abstract
Following lung transplantation, fibrotic remodelling of the small airways has been recognized for almost 5 decades as the main correlate of chronic graft failure and a major obstacle to long-term survival. Mainly due to airway fibrosis, pulmonary allografts currently show the highest attrition rate of all solid organ transplants, with a 5-year survival rate of 58 % on a worldwide scale. The observation that these morphological changes are not just the hallmark of chronic rejection but rather represent a manifestation of a multitude of alloimmune-dependent and -independent injuries was made more recently, as was the discovery that chronic lung allograft dysfunction manifests in different clinical phenotypes of respiratory impairment and corresponding morphological subentities. Although recent years have seen considerable advances in identifying and categorizing these subgroups on the basis of clinical, functional and histomorphological changes, as well as susceptibility to medicinal treatment, this process is far from over. Since the actual pathophysiological mechanisms governing airway remodelling are still only poorly understood, diagnosis and therapy of chronic lung allograft dysfunction presents a major challenge to clinicians, radiologists and pathologists alike. Here, we review and discuss the current state of the literature on chronic lung allograft dysfunction and shed light on classification systems, corresponding clinical and morphological changes, key cellular players and underlying molecular pathways, as well as on emerging diagnostic and therapeutic approaches.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1-13 |
| Number of pages | 13 |
| Journal | Cell and Tissue Research |
| DOIs | |
| State | Accepted/In press - Nov 12 2016 |
| Externally published | Yes |
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Keywords
- Bronchiolitis obliterans
- Chronic lung allograft dysfunction
- Chronic rejection
- Lung transplantation
- Obliterative airway remodelling
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Histology
- Cell Biology
Cite this
Airway remodelling in the transplanted lung. / Kuehnel, Mark; Maegel, Lavinia; Vogel-Claussen, Jens; Robertus, Jan Lukas; Jonigk, Danny.
In: Cell and Tissue Research, 12.11.2016, p. 1-13.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Airway remodelling in the transplanted lung
AU - Kuehnel, Mark
AU - Maegel, Lavinia
AU - Vogel-Claussen, Jens
AU - Robertus, Jan Lukas
AU - Jonigk, Danny
PY - 2016/11/12
Y1 - 2016/11/12
N2 - Following lung transplantation, fibrotic remodelling of the small airways has been recognized for almost 5 decades as the main correlate of chronic graft failure and a major obstacle to long-term survival. Mainly due to airway fibrosis, pulmonary allografts currently show the highest attrition rate of all solid organ transplants, with a 5-year survival rate of 58 % on a worldwide scale. The observation that these morphological changes are not just the hallmark of chronic rejection but rather represent a manifestation of a multitude of alloimmune-dependent and -independent injuries was made more recently, as was the discovery that chronic lung allograft dysfunction manifests in different clinical phenotypes of respiratory impairment and corresponding morphological subentities. Although recent years have seen considerable advances in identifying and categorizing these subgroups on the basis of clinical, functional and histomorphological changes, as well as susceptibility to medicinal treatment, this process is far from over. Since the actual pathophysiological mechanisms governing airway remodelling are still only poorly understood, diagnosis and therapy of chronic lung allograft dysfunction presents a major challenge to clinicians, radiologists and pathologists alike. Here, we review and discuss the current state of the literature on chronic lung allograft dysfunction and shed light on classification systems, corresponding clinical and morphological changes, key cellular players and underlying molecular pathways, as well as on emerging diagnostic and therapeutic approaches.
AB - Following lung transplantation, fibrotic remodelling of the small airways has been recognized for almost 5 decades as the main correlate of chronic graft failure and a major obstacle to long-term survival. Mainly due to airway fibrosis, pulmonary allografts currently show the highest attrition rate of all solid organ transplants, with a 5-year survival rate of 58 % on a worldwide scale. The observation that these morphological changes are not just the hallmark of chronic rejection but rather represent a manifestation of a multitude of alloimmune-dependent and -independent injuries was made more recently, as was the discovery that chronic lung allograft dysfunction manifests in different clinical phenotypes of respiratory impairment and corresponding morphological subentities. Although recent years have seen considerable advances in identifying and categorizing these subgroups on the basis of clinical, functional and histomorphological changes, as well as susceptibility to medicinal treatment, this process is far from over. Since the actual pathophysiological mechanisms governing airway remodelling are still only poorly understood, diagnosis and therapy of chronic lung allograft dysfunction presents a major challenge to clinicians, radiologists and pathologists alike. Here, we review and discuss the current state of the literature on chronic lung allograft dysfunction and shed light on classification systems, corresponding clinical and morphological changes, key cellular players and underlying molecular pathways, as well as on emerging diagnostic and therapeutic approaches.
KW - Bronchiolitis obliterans
KW - Chronic lung allograft dysfunction
KW - Chronic rejection
KW - Lung transplantation
KW - Obliterative airway remodelling
UR - http://www.scopus.com/inward/record.url?scp=84994719173&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84994719173&partnerID=8YFLogxK
U2 - 10.1007/s00441-016-2529-0
DO - 10.1007/s00441-016-2529-0
M3 - Article
SP - 1
EP - 13
JO - Cell and Tissue Research
JF - Cell and Tissue Research
SN - 0302-766X
ER -