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Macrophage effector function in pulmonary oxygen toxicity: hyperoxia damages and stimulates alveolar macrophages to
Abstract:
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.
Insights
Hyperoxia damages rabbit alveolar macrophages (AM), causing them to release substances that attract polymorphonuclear leukocytes (PMN). This suggests AM secretions are vital in lung inflammation during oxygen toxicity.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Toxicology
Background:
- Macrophages produce various secretions, but triggers and in vivo significance remain unclear.
- Pulmonary oxygen toxicity is a condition where high oxygen levels damage lung tissue.
Purpose of the Study:
- To investigate the effects of hyperoxia on rabbit alveolar macrophages (AM).
- To determine if hyperoxia-induced AM damage and secretions contribute to lung inflammation.
Main Methods:
- Cultured rabbit AM were exposed to hyperoxia in vitro.
- Cell viability, lactate dehydrogenase (LDH) release, and ultrastructural changes were assessed.
- Chemotactic factors released by AM were analyzed and compared to those from in vivo hyperoxia exposure.
Main Results:
- Hyperoxia exposure in vitro led to decreased AM numbers, increased LDH release, and cellular damage.
- Cultured AM exposed to hyperoxia released chemotaxins for polymorphonuclear leukocytes (PMN).
- These chemotaxins were similar in molecular weight to those found in vivo.
Conclusions:
- Hyperoxia damages rabbit AM in vitro and in vivo.
- AM secretory products, stimulated by hyperoxia, may recruit PMN to the lungs.
- This highlights a potential role for AM in pulmonary oxygen toxicity.