Abstract
Background: The loss of a normal airway is devastating. Attempts to replace large airways have met with serious problems. Prerequisites for a tissue-engineered replacement are a suitable matrix, cells, ideal mechanical properties, and the absence of antigenicity. We aimed to bioengineer tubular tracheal matrices, using a tissue-engineering protocol, and to assess the application of this technology in a patient with end-stage airway disease. Methods: We removed cells and MHC antigens from a human donor trachea, which was then readily colonised by epithelial cells and mesenchymal stem-cell-derived chondrocytes that had been cultured from cells taken from the recipient (a 30-year old woman with end-stage bronchomalacia). This graft was then used to replace the recipient's left main bronchus. Findings: The graft immediately provided the recipient with a functional airway, improved her quality of life, and had a normal appearance and mechanical properties at 4 months. The patient had no anti-donor antibodies and was not on immunosuppressive drugs. Interpretation: The results show that we can produce a cellular, tissue-engineered airway with mechanical properties that allow normal functioning, and which is free from the risks of rejection. The findings suggest that autologous cells combined with appropriate biomaterials might provide successful treatment for patients with serious clinical disorders. Funding: Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III, Fondo de Investigación Sanitaria, Spain; Charles Courtenay-Cowlin Fund, University of Bristol; UK Arthritis Research Campaign; and the James Tudor Foundation.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2023-2030 |
| Number of pages | 8 |
| Journal | The Lancet |
| Volume | 372 |
| Issue number | 9655 |
| DOIs | |
| State | Published - 2008 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Medicine(all)
Cite this
Clinical transplantation of a tissue-engineered airway. / Macchiarini, Paolo; Jungebluth, Philipp; Go, Tetsuhiko; Asnaghi, M. Adelaide; Rees, Louisa E.; Cogan, Tristan A.; Dodson, Amanda; Martorell, Jaume; Bellini, Silvia; Parnigotto, Pier Paolo; Dickinson, Sally C.; Hollander, Anthony P.; Mantero, Sara; Conconi, Maria Teresa; Birchall, Martin A.
In: The Lancet, Vol. 372, No. 9655, 2008, p. 2023-2030.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Clinical transplantation of a tissue-engineered airway
AU - Macchiarini, Paolo
AU - Jungebluth, Philipp
AU - Go, Tetsuhiko
AU - Asnaghi, M. Adelaide
AU - Rees, Louisa E.
AU - Cogan, Tristan A.
AU - Dodson, Amanda
AU - Martorell, Jaume
AU - Bellini, Silvia
AU - Parnigotto, Pier Paolo
AU - Dickinson, Sally C.
AU - Hollander, Anthony P.
AU - Mantero, Sara
AU - Conconi, Maria Teresa
AU - Birchall, Martin A.
PY - 2008
Y1 - 2008
N2 - Background: The loss of a normal airway is devastating. Attempts to replace large airways have met with serious problems. Prerequisites for a tissue-engineered replacement are a suitable matrix, cells, ideal mechanical properties, and the absence of antigenicity. We aimed to bioengineer tubular tracheal matrices, using a tissue-engineering protocol, and to assess the application of this technology in a patient with end-stage airway disease. Methods: We removed cells and MHC antigens from a human donor trachea, which was then readily colonised by epithelial cells and mesenchymal stem-cell-derived chondrocytes that had been cultured from cells taken from the recipient (a 30-year old woman with end-stage bronchomalacia). This graft was then used to replace the recipient's left main bronchus. Findings: The graft immediately provided the recipient with a functional airway, improved her quality of life, and had a normal appearance and mechanical properties at 4 months. The patient had no anti-donor antibodies and was not on immunosuppressive drugs. Interpretation: The results show that we can produce a cellular, tissue-engineered airway with mechanical properties that allow normal functioning, and which is free from the risks of rejection. The findings suggest that autologous cells combined with appropriate biomaterials might provide successful treatment for patients with serious clinical disorders. Funding: Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III, Fondo de Investigación Sanitaria, Spain; Charles Courtenay-Cowlin Fund, University of Bristol; UK Arthritis Research Campaign; and the James Tudor Foundation.
AB - Background: The loss of a normal airway is devastating. Attempts to replace large airways have met with serious problems. Prerequisites for a tissue-engineered replacement are a suitable matrix, cells, ideal mechanical properties, and the absence of antigenicity. We aimed to bioengineer tubular tracheal matrices, using a tissue-engineering protocol, and to assess the application of this technology in a patient with end-stage airway disease. Methods: We removed cells and MHC antigens from a human donor trachea, which was then readily colonised by epithelial cells and mesenchymal stem-cell-derived chondrocytes that had been cultured from cells taken from the recipient (a 30-year old woman with end-stage bronchomalacia). This graft was then used to replace the recipient's left main bronchus. Findings: The graft immediately provided the recipient with a functional airway, improved her quality of life, and had a normal appearance and mechanical properties at 4 months. The patient had no anti-donor antibodies and was not on immunosuppressive drugs. Interpretation: The results show that we can produce a cellular, tissue-engineered airway with mechanical properties that allow normal functioning, and which is free from the risks of rejection. The findings suggest that autologous cells combined with appropriate biomaterials might provide successful treatment for patients with serious clinical disorders. Funding: Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III, Fondo de Investigación Sanitaria, Spain; Charles Courtenay-Cowlin Fund, University of Bristol; UK Arthritis Research Campaign; and the James Tudor Foundation.
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UR - http://www.scopus.com/inward/citedby.url?scp=57349176894&partnerID=8YFLogxK
U2 - 10.1016/S0140-6736(08)61598-6
DO - 10.1016/S0140-6736(08)61598-6
M3 - Article
C2 - 19022496
AN - SCOPUS:57349176894
VL - 372
SP - 2023
EP - 2030
JO - The Lancet
JF - The Lancet
SN - 0140-6736
IS - 9655
ER -