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The immunopathology of pulmonary rejection after murine lung transplantation.
Cells 13:241 (2024)
To improve outcomes following lung transplantation, it is essential to understand the immunological mechanisms that result in chronic graft failure. The associated clinical syndrome is termed chronic lung allograft dysfunction (CLAD), which is known to be induced by alloimmune-dependent (i.e., rejection) and alloimmune-independent factors (e.g., infections, reflux and environmental factors). We aimed to explore the alloimmune-related mechanism, i.e., pulmonary rejection. In this study, we use a murine orthotopic left lung transplant model using isografts and allografts (C57BL/6 or BALB/c as donors to C57BL/6 recipients), with daily immunosuppression (10 mg/kg cyclosporin A and 1.6 mg/kg methylprednisolone). Serial sacrifice was performed at days 1, 7 and 35 post-transplantation (n = 6 at each time point for each group). Left transplanted lungs were harvested, a single-cell suspension was made and absolute numbers of immune cells were quantified using multicolor flow cytometry. The rejection process followed the principles of a classic immune response, including innate but mainly adaptive immune cells. At day 7 following transplantation, the numbers of interstitial macrophages, monocytes, dendritic cells, NK cells, NKT cells, CD4+ T cells and CD8+ T and B cells were increased in allografts compared with isografts. Only dendritic cells and CD4+ T cells remained elevated at day 35 in allografts. Our study provides insights into the immunological mechanisms of true pulmonary rejection after murine lung transplantation. These results might be important in further research on diagnostic evaluation and treatment for CLAD.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Chronic Lung Allograft Dysfunction (clad) ; Immunology ; Lung Transplantation ; Murine Orthotopic Left Lung Transplantation ; Pulmonary Rejection; Bronchoalveolar Lavage; Allograft Dysfunction; Phenotypes; Mechanisms; Update; Model
ISSN (print) / ISBN
2073-4409
e-ISSN
2073-4409
Zeitschrift
Cells
Quellenangaben
Band: 13,
Heft: 3,
Artikelnummer: 241
Verlag
MDPI
Verlagsort
Basel
Nichtpatentliteratur
Publikationen
Institut(e)
Institute of Lung Biology (LHI)
Förderungen
FWO