BAL levels of interleukin-18 do not change before or during acute rejection in lungtransplant recipients

Study objective: Acute rejection (AR) of the allograft is a major clinical problem after lungtransplantation. Repeated episodes of AR increase the risk of developing obliterative bronchiolitis, the main cause of mortality in this patient group. It is believed that AR is caused by T-lymphocytes react...

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Veröffentlicht in:Respiratory medicine 2004-02, Vol.98 (2), p.159-163
Hauptverfasser: Ericson, Petrea, Lindén, Anders, Riise, Gerdt C
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Sprache:eng
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Zusammenfassung:Study objective: Acute rejection (AR) of the allograft is a major clinical problem after lungtransplantation. Repeated episodes of AR increase the risk of developing obliterative bronchiolitis, the main cause of mortality in this patient group. It is believed that AR is caused by T-lymphocytes reacting to donor antigens and in turn activating antigen presenting cells (APC) such as alveolar macrophages. Hypothetically, the interferon- γ inducing cytokine IL-18 released from activated macrophages can play a role in the development of AR by modulating cytotoxic T-lymphocytes. Design: To determine whether IL-18 may serve as a marker of AR, we retrospectively analysed the concentration of soluble IL-18 protein and inflammatory cells in bronchoalveolar lavage fluid (BAL) from lungtransplant recipients. Patients: To minimize confounding factors, eight pairs of patients were matched for age, gender, pre-op diagnosis, type of operation, absence of infection and time post transplant. Methods: BAL levels of IL-18 (ELISA) and BAL cell differentials were analysed before, during and after an episode of AR and compared with the matched control group. Conclusion: We found no changes in IL-18 concentration in BAL associated with AR. IL-18 in BAL did not correlate with BAL lymphocyte percentage. We conclude that change in soluble IL-18 protein does not constitute a useful marker of acute rejection in lung allograft recipients.
ISSN:0954-6111
1532-3064
DOI:10.1016/j.rmed.2003.09.007