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Marked stem cell factor expression in the airways of lung transplant recipients

Carla A Da Silva1 email, Mélanie Adda2 email, Marc Stern3 email, Frédéric de Blay1 email, Nelly Frossard1 email and Dominique Israel-Biet2,4 email

1EA 3771 'Inflammation and environment in asthma'. Faculté de Pharmacie, BP 60024, 67401 Illkirch Cedex, France

UPRES EA 220. Université Paris V. UFR Biomédicale des Saints-Pères, 45 rue des Saints-Pères, 75006 Paris, France

Service de Pneumologie. CMC Foch, 40 rue Worth, 92151 Suresnes Cedex, France

Service de Pneumologie. Hôpital Européen Georges Pompidou, Faculté de Médecine Paris V, 20 rue Leblanc, 75015 Paris, France

author email corresponding author email

Respiratory Research 2006, 7:90doi:10.1186/1465-9921-7-90

Published: 16 June 2006

Abstract

Background

Airways repair is critical to lung function following transplantation. We hypothesised that the stem cell factor (SCF) could play a role in this setting.

Methods

We studied 9 lung transplant recipients (LTx recipients) during their first year postgraft, and evaluated SCF mRNA expression in bronchial biopsy specimens using on-line fluorescent PCR and SCF protein levels in bronchoalveolar lavage (BAL) and serum using ELISA. The expression of SCF receptor Kit was assessed using immunostaining of paraffin-embedded bronchial sections.

Results

SCF mRNA was highly expressed during the early postgraft period [Month (M)1-M3] (300% increase vs controls: 356 vs 1.2 pg SCF/μg GAPDH cDNA, p < 0.001) and decreased thereafter (M4-M12: 187 pg/μg), although remaining at all times 10–100 times higher than in controls. While SCF protein levels in BAL were similar in LTx recipients and in controls, the SCF serum levels were at all times higher in LTx recipients than in controls (p < 0.05), with no relationship between these levels and the acute complications of the graft. Finally, Kit was strongly expressed by the mast cells as well as by the bronchial epithelium of LTx recipients.

Conclusion

SCF and Kit are expressed in bronchial biopsies from lung transplant recipients irrespective of the clinical status of the graft. A role for these factors in tissue repair following lung transplantation is hypothesised.


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