LUNG INJURY INDUCED BY ANTIBODY FRAGMENTS TO ANGIOTENSIN-CONVERTING ENZYME

  • 1 January 1981
    • journal article
    • research article
    • Vol. 105  (1) , 54-63
Abstract
Rabbits given goat anti-rabbit angiotensin-converting enzyme [ACE] antibodies or derived antibody fragments develop rapidly fatal pulmonary edema. Endothelial cell injury is manifested by bleb formation and the disintegration of cell membranes. Platelets are found along the injured endothelium and leukocytes block capillary lumens. The pathologic features are similar when immune IgG, F(ab'')2, or Fab are given. In vitro studies of complement activation show that solubilized, purified ACE alone activates C1 [complement component 1], with consumption of C4 and C3. Addition of immune IgG plus ACE enhances this activation. F(ab'')2 plus ACE enhances only C3 consumption; Fab with ACE produces no additional complement utilization. Thus, while complement activation may be involved in the pathogenesis of injury induced by IgG or F(ab'')2, the mechanism of Fab-induced endothelial injury remains unclear.