Allogeneic bronchoalveolar lavage cells induce the histology and immunology of lung allograft rejection in recipient murine lungs: role of intercellular adhesion molecule-1 on donor cells

• Published in: Transplantation Vol. 67; no. 6; p. 890
• Main Authors: Wilkes, D S, Bowman, D, Cummings, O W, Heidler, K M
• Format: Journal Article
• Language: English
• Published: United States 27.03.1999
• Subjects: Animals; Bronchoalveolar Lavage Fluid - cytology; Graft Rejection; Immunoglobulin G - blood; Immunoglobulin G - classification; Intercellular Adhesion Molecule-1 - physiology; Interferon-gamma - biosynthesis; Lung - immunology; Lung - pathology; Lung Transplantation - immunology; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Transplantation, Homologous
• ISSN: 0041-1337
• DOI: 10.1097/00007890-199903270-00017

Intercellular adhesion molecule (ICAM)-1 expressed on accessory cells has a key role in antigen presentation. The histology and immunology of lung allograft rejection is postulated to result from donor lung accessory cells presenting alloantigens to recipient lymphocytes, and, therefore, ICAM-1 may have a crucial role in the rejection process. We have previously reported that the instillation of allogeneic (C57BL/6, I-a(b)) bronchoalveolar lavage (BAL) cells (96% macrophages, 2% dendritic cells) into the lungs of recipient BALB/c mice (I-a(d)) induced the histology and immunology of acute lung allograft rejection. Using this model, the purpose of the current study was to determine the role of ICAM-1 on donor lung cells in lung allograft rejection. BALB/c mice received allogeneic BAL cells from wild-type or ICAM-1 mutant (lacking ICAM-1 expression) C57BL/6 mice by nasal insufflation weekly for 4 weeks. Recipient mice underwent BAL and serum collection for the determination of T helper 1/T helper 2 cytokines and IgG subtypes. Lung histology was graded using standard criteria for allograft rejection. Although wild-type cells induced a lymphocytic vasculitis and bronchitis, ICAM-1 mutant allogeneic BAL cells only induced a lymphocytic vasculitis in recipient lungs. Both wild-type and ICAM-1 mutant cells induced up-regulated local interferon-gamma and IgG2a production, and deposition of IgG2a in recipient lungs. These data show that ICAM-1 on donor lung accessory cells mediates differential effects on the histology and immunology of acute lung allograft rejection.