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

Am Rev Respir Dis. 1992 May;145(5):1155-9. doi: 10.1164/ajrccm/145.5.1155.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bronchoalveolar Lavage Fluid / cytology
  • Graft Rejection / immunology*
  • Lung Transplantation / immunology*
  • Macrophages, Alveolar / metabolism*
  • Male
  • Neutrophils / metabolism*
  • Rats
  • Rats, Inbred BN
  • Rats, Inbred Lew
  • Superoxides / metabolism*

Substances

  • Superoxides