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

David S. Wilkes, David Bowman, Oscar Cummings, Kathleen M. Heidler

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background. 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-ab) 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. Methods. 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. Results. 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-γ and IgG2a production, and deposition of IgG2a in recipient lungs. Conclusions. These data show that ICAM-1 on donor lung accessory cells mediates differential effects on the histology and immunology of acute lung allograft rejection.

Original languageEnglish
Pages (from-to)890-896
Number of pages7
JournalTransplantation
Volume67
Issue number6
StatePublished - Mar 27 1999

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Therapeutic Irrigation
Intercellular Adhesion Molecule-1
Allergy and Immunology
Allografts
Histology
Lung
Bronchoalveolar Lavage
Vasculitis
Insufflation
Isoantigens
Bronchitis
Antigen Presentation
Cell Adhesion Molecules
Inbred C57BL Mouse
Nose
Dendritic Cells
Interferons
Immunoglobulin G
Macrophages
Lymphocytes

ASJC Scopus subject areas

  • Immunology
  • Transplantation

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Allogeneic bronchoaleolar lavage cells induce the histology and immunology of lung allograft rejection in recipient murine lungs : Role of intercellular adhesion molecule-1 on donor cells. / Wilkes, David S.; Bowman, David; Cummings, Oscar; Heidler, Kathleen M.

In: Transplantation, Vol. 67, No. 6, 27.03.1999, p. 890-896.

Research output: Contribution to journalArticle

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abstract = "Background. 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-ab) 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. Methods. 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. Results. 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-γ and IgG2a production, and deposition of IgG2a in recipient lungs. Conclusions. These data show that ICAM-1 on donor lung accessory cells mediates differential effects on the histology and immunology of acute lung allograft rejection.",
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