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Copyright ©ERS Journals Ltd 2006
The role of interleukin-17 during acute rejection after lung transplantation
1 Laboratory of Pneumology and, 2 Laboratory of Immunology, Katholieke Universiteit, 3 Lung Transplantation Unit and, 4 Dept of Histopathology, University Hospital Gasthuisberg, Leuven, Belgium.
CORRESPONDENCE: G. M. Verleden, Dept Respiratory Disease and Lung Transplantation Unit, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium. Fax: 32 16346803. E-mail: geert.verleden{at}uz.kuleuven.ac.be
Keywords: Acute rejection, bronchoalveolar lavage, interleukin-17, interleukin-8, lung transplantation, neutrophils
Received: February 19, 2005
Accepted December 12, 2005
Acute rejection (AR) is an important complication that can occur after lung transplantation and constitutes a risk factor for bronchiolitis obliterans syndrome, which is characterised by a neutrophilic airway inflammation. The specific aim of this study was to investigate the role of interleukin (IL)-17, which promotes chemotaxis of neutrophils by inducing IL-8 production, in AR.
Cell differentials, mRNA and protein levels were quantified in bronchoalveolar lavages (BALs) taken from patients at 28 and 90 days after lung transplantation. The patient's rejection status was assessed by transbronchial biopsy.
An AR was found in nine out of the 26 patients examined, 28 days after transplantation. The number of BAL neutrophils and lymphocytes were increased in these patients. IL-17 mRNA and protein levels in the BAL were increased in patients with AR. Analysis of BAL obtained at day 90 after transplantation, demonstrated that the increase in IL-17 had disappeared, whereas the increase in neutrophils and lymphocytes persisted.
These data showed that interleukin-17 is temporarily upregulated in bronchoalveolar lavage during acute rejection. The number of lymphocytes and neutrophils are increased in bronchoalveolar lavage during acute rejection and may persist up to 2 months after acute rejection. These findings suggest that interleukin-17 is important in the pathophysiology of acute lung rejection.
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