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Airway epithelial cell senescence in the lung allograft

Lookup NU author(s): Dr Sean Parker, Dr Lee Borthwick, Professor Christopher WardORCiD, Dr James Lordan, Emeritus Professor Nick Europe-Finner, Dr Gabriele Saretzki, Professor Andrew FisherORCiD


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Chronic lung allograft dysfunction, manifesting as bronchiolitis obliterans syndrome (BOS), is characterized by airway epithelial injury, impaired epithelial regeneration and subsequent airway remodeling. Increased cellular senescence has been reported in renal and liver allografts affected by chronic allograft dysfunction but the significance of cellular senescence in the airway epithelium of the transplanted lung is unknown. Thirty-four lung transplant recipients, 20 with stable graft function and 14 with BOS, underwent transbronchial lung biopsy and histochemical studies for senescence markers in small airways. Compared to nontransplant control lung tissue (n = 9), lung allografts demonstrate significantly increased airway epithelial staining for senescence-associated beta galactosidase (SA β-gal) (p = 0.0215), p16 ink4a (p = 0.0002) and p21waf1/cip (p = 0.0138) but there was no difference in expression of these markers between stable and BOS affected recipients (p > 0.05). This preliminary cross-sectional study demonstrates that cellular senescence occurs with increased frequency in the airway epithelium of the lung allograft but does not establish any association between airway epithelial senescence and BOS. A prospective longitudinal study is required to better address any potential causal association between airway epithelial senescence in stable allograft recipients and the subsequent development of BOS. © 2008 The Authors.

Publication metadata

Author(s): Parker SM, Goriwiec MR, Borthwick LA, Johnson G, Ward C, Lordan JL, Corris PA, Saretzki GC, Fisher AJ

Publication type: Article

Publication status: Published

Journal: American Journal of Transplantation

Year: 2008

Volume: 8

Issue: 7

Pages: 1544-1549

ISSN (print): 1600-6135

ISSN (electronic): 1600-6143

Publisher: Wiley-Blackwell Publishing Ltd.


DOI: 10.1111/j.1600-6143.2008.02284.x


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