Expression of ICAM-1 and TNF? in Human Alveolar Macrophages from Lung-Transplant Recipients
- 1 October 1996
- journal article
- Published by Wiley in Annals of the New York Academy of Sciences
- Vol. 796 (1 Cytokine), 138-148
- https://doi.org/10.1111/j.1749-6632.1996.tb32575.x
Abstract
Local activation of macrophages may play an important role in the immune process of pulmonary infections and in the inflammatory response of lung allograft rejection. To document macrophage activation within human lung allografts displaying various complications, we have investigated ICAM-1 expression in freshly isolated alveolar macrophages (AM) from lung-transplant recipients by immunocytofluorimetric analysis, and rIFN gamma induced in vitro by ELISA. A total of 21 bronchoalveolar lavage fluids (BAL) from 13 transplanted patients displaying no complication, acute rejection, bacterial/fungal infection, or CMV infection entered the study. ICAM-1 was expressed at a higher level in rejecting patients. Surprisingly, TNF alpha release from AM upon in vitro activation was significantly decreased during rejection. Furthermore, we have studied the effects of the glucocorticoid dexamethasone, the key drug for the treatment of allograft rejection, on the expression of ICAM-1 and TNF alpha induced in vitro in AM, at the levels of protein production and of transcription. Whereas dexamethasone did not influence ICAM-1 expression in AM, it downregulated TNF alpha production at least in part at the transcriptional level. Our results suggest strongly that the anti-inflammatory effects of corticosteroids are not related to ICAM-1 modulation on human AM but to the downregulation of the proinflammatory cytokine TNF alpha that is produced early in the inflammatory process. Moreover, our model of human AM activation induced in vitro by rIFN gamma appears a useful tool for in vitro investigation of the cellular and molecular targets of anti-inflammatory drugs for a more appropriate use.This publication has 13 references indexed in Scilit:
- Interleukin-10 and the Monocyte/Macrophage-Induced Inflammatory Response in Septic ShockThe Journal of Infectious Diseases, 1995
- EMERGENCE OF INFLAMMATORY ALVEOLAR MACROPHAGES DURING REJECTION OR INFECTION AFTER LUNG TRANSPLANTATIONTransplantation, 1994
- Intercellular adhesion molecule-1 (ICAM-1) is upregulated on alveolar macrophages from AIDS patientsEuropean Respiratory Journal, 1994
- Cytokines and macrophagesBiomedicine & Pharmacotherapy, 1994
- Intercellular adhesion molecule 1 (ICAM-1) in the pathogenesis of mononuclear cell alveolitis in pulmonary sarcoidosis.Thorax, 1993
- IN SITU PRODUCTION OF INTERLEUKIN-6 WITHIN HUMAN LUNG ALLOGRAFTS DISPLAYING REJECTION OR CYTOMEGALOVIRUS PNEUMONIATransplantation, 1993
- Corticosteroids induce proliferation but do not influence TNF- or IL-1?-induced ICAM-1 expression of human dermal microvascular endothelial cells in vitroArchives of Dermatological Research, 1993
- Expression of Alveolar Macrophage Adhesion Molecules in Pulmonary SarcoidosisChest, 1992
- Expression and function of intercellular adhesion molecule 1 (ICAM-1) on rat thymic macrophages in cultureImmunology Letters, 1991
- ICAM, an adhesion ligand of LFA-1, is homologous to the neural cell adhesion molecule NCAMNature, 1988