Premium
Macrophage Effector Function in Pulmonary Oxygen Toxicity: Hyperoxia Damages and Stimulates Alveolar Macrophages to Make and Release Chemotaxins for Polymorphonuclear Leukocytes
Author(s) -
Harada Ruth N.,
Vatter Albert E.,
Repine John E.
Publication year - 1984
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.35.4.373
Subject(s) - hyperoxia , in vivo , alveolar macrophage , biology , macrophage , oxygen toxicity , pulmonary alveolus , in vitro , lung , lactate dehydrogenase , effector , toxicity , immunology , biochemistry , medicine , enzyme , microbiology and biotechnology
Macrophages synthesize many secretory products in vitro but the stimuli for their production and their pathophysiologic significance in vivo are largely unknown. In the present investigation, we found that hyperoxia damaged rabbit alveolar macrophages (AM) in vitro as manifested by decreased cell numbers, increased lactate dehydrogenase (LDH) release, and the development of ultrastructural abnormalities that resembled those seen in AM in situ or lavaged from lungs of rabbits exposed to hyperoxia in vivo. Hyperoxia also stimulated cultured rabbit AM to release chemotaxins for polymorphonuclear leukocytes (PMN) that were similar in molecular weight to chemotaxins obtained from lung lavages of rabbits exposed to hyperoxia in vivo. Our results suggest that alveolar macrophage secretory products may play a physiologically relevant role in recruitment of PMN to the lungs in pulmonary oxygen toxicity.