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THERE IS NO ACTIVATION OF O2- PRODUCTION BY ALVEOLAR MACROPHAGES AND NEUTROPHIL POLYMORPHONUCLEAR LEUKOCYTES IN RAT LUNG TRANSPLANTS DURING THE REIMPLANTATION RESPONSE AND ACUTE REJECTION

OOSTERHOFF, Y., NOORDHOEK, JA., PETERSEN, AH., KAUFFMAN, HF., POSTMA, DS. & PROP, J., May-1992, In : American Review of Respiratory Disease. 145, 5, p. 1155-1159 5 p.

Research output: Contribution to journalArticleAcademicpeer-review

Activation of phagocytes (alveolar macrophages [AM] and neutrophil polymorphonuclear leukocytes [PMN]) can cause tissue damage in inflammatory lung diseases. in this study we investigated whether phagocytes contribute to the development of tissue damage in lung grafts histologically observed during two different processes: the reimplantation response and the acute rejection. Therefore, the number and profile of bronchoalveolar lavage (BAL) and blood phagocytes and their in vitro spontaneous and serum-treated-zymosan (STZ)-stimulated O2- production were assessed after allogeneic (BN to LEW) and syngeneic (LEW to LEW) transplantation of the left lung in rats. BAL PMN numbers increased during the reimplantation response, whereas during the late phase of the rejection process BAL AM and PMN numbers were increased. The O2- production by the BAL phagocytes and blood PMN were not increased at any stage. Strikingly, the STZ-stimulated O2- production by the BAL phagocytes was significantly impaired during acute rejection. Our data suggest that activation of the O2- production by bronchoalveolar phagocytes does not play an important role in the development of tissue damage in lung transplants during the reimplantation response and acute rejection. The impaired O2- production by alveolar phagocytes during acute lung rejection may contribute to the increased susceptibility for pulmonary infections after lung transplantation.

Original languageEnglish
Pages (from-to)1155-1159
Number of pages5
JournalAmerican Review of Respiratory Disease
Volume145
Issue number5
Publication statusPublished - May-1992

    Keywords

  • SUPEROXIDE ANION, INJURY, MECHANISMS, INFECTION, DEFENSE

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