Donor-derived TNF-α regulates pulmonary chemokine expression and the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation
| العنوان: | Donor-derived TNF-α regulates pulmonary chemokine expression and the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation |
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| المؤلفون: | Shawn G. Clouthier, Krystyna M. Olkiewicz, Yayi Chang, Gerhard C. Hildebrandt, Leigh A. Corrion, Chen Liu, Kenneth R. Cooke |
| المصدر: | Blood. 104:586-593 |
| بيانات النشر: | American Society of Hematology, 2004. |
| سنة النشر: | 2004 |
| مصطلحات موضوعية: | Chemokine, T-Lymphocytes, medicine.medical_treatment, Immunology, Inflammation, Lung injury, Biochemistry, Mice, Idiopathic pneumonia syndrome, medicine, Animals, Transplantation, Homologous, Lung, Cells, Cultured, Bone Marrow Transplantation, biology, medicine.diagnostic_test, Tumor Necrosis Factor-alpha, business.industry, Pneumonia, Cell Biology, Hematology, medicine.disease, Mice, Mutant Strains, Mice, Inbred C57BL, Transplantation, Bronchoalveolar lavage, Cytokine, biology.protein, Female, Tumor necrosis factor alpha, Chemokines, medicine.symptom, business |
| الوصف: | Idiopathic pneumonia syndrome (IPS) is a significant cause of mortality after allogeneic bone marrow transplantation (allo-BMT), and tumor necrosis factor-α (TNF-α) is a significant effector molecule in this process. However, the relative contribution of donor-versus host-derived TNF-α to the development of IPS has not been elucidated. Using a lethally irradiated parent → F1 mouse IPS model, we showed that 5 weeks after transplantation allo-BMT recipients developed significant lung injury compared with syngeneic controls, which was associated with increased bronchoalveolar lavage (BAL) fluid levels of TNF-α, elevated numbers of donor-derived TNF-α-secreting T cells, and increased pulmonary macrophage production of TNF-α to lipopolysaccharide (LPS) stimulation. Allo-BMT with TNF-α-/- donor cells resulted in significantly reduced IPS severity, whereas utilization of TNF-α-deficient mice as BMT recipients had no effect on IPS. We next determined that TNF-α secretion from both donor accessory cells (monocytes/macrophages) and T cells significantly contributed to the development of IPS. Importantly, the absence of donor T-cell-derived TNF-α resulted in a significant decrease in inflammatory chemokine production in the lung and near complete abrogation of IPS. Collectively, these data demonstrate that donor TNF-α is critical to the development of IPS and reveal a heretofore unknown mechanism for T-cell-derived TNF-α in the evolution of this process. (Blood. 2004;104:586-593) |
| تدمد: | 1528-0020 0006-4971 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::704e4d224e2a0e122420cded07cda8f8 https://doi.org/10.1182/blood-2003-12-4259 |
| رقم الأكسشن: | edsair.doi.dedup.....704e4d224e2a0e122420cded07cda8f8 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15280020 00064971 |
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