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Smoking decreases alveolar macrophage function during anesthesia and surgery
N Kotani1, H Hashimoto, D I Sessler
1Department of Anesthesiology, University of Hirosaki, Hirosaki 036-8562, Japan. nao@cc.hirosaki-u.ac.jp
Background:
Smoking changes numerous alveolar macrophage functions and is one of the most important risk factors for postoperative pulmonary complications. The current study tested the hypothesis that smoking impairs antimicrobial and proinflammatory responses in alveolar macrophages during anesthesia and surgery.
Method:
The authors studied 30 smoking and 30 nonsmoking patients during propofol-fentanyl general anesthesia. Alveolar immune cells were harvested by bronchoalveolar lavage immediately and 2, 4, and 6 h after induction of anesthesia and at the end of surgery. The types of alveolar immune cell and macrophage aggregation were determined. The authors measured opsonized and unopsonized phagocytosis. Microbicidal activity was determined as the ability of the macrophages to kill Listeriamonocytogenes directly. Finally, RNA was extracted from harvested cells and cDNA was synthesized by reverse transcription. The expression of interleukin 1beta, 6, and 8, interferon gamma, and tumor necrosis factor alpha were measured by semiquantitative polymerase chain reaction using beta-actin as an internal standard.
Results:
The fraction of aggregated macrophages increased significantly over time in both groups, whereas phagocytosis of opsonized and nonopsonized particles and microbicidal activity of alveolar macrophages decreased significantly. The changes, though, were nearly twice as great as in patients who smoked. Gene expression of all proinflammatory cytokines in alveolar immune cells except interleukin 6 increased 2- to 20-fold over time in both groups. The expression of interleukin 1beta, interferon gamma, and tumor necrosis factor alpha, however, increased only half as much in smokers as in nonsmokers.
Conclusion:
Smoking was associated with macrophage aggregation but markedly reduced phagocytic and microbicidal activity-possibly because expression of proinflammatory cytokines was reduced in these patients. Our data thus suggest that smokers may have a limited ability to mount an effective pulmonary immune defense after anesthesia and surgery.
Insights
Smoking impairs pulmonary immune defenses after surgery. Smokers showed reduced macrophage activity and lower cytokine responses, suggesting a limited ability to fight infection post-anesthesia.
Area of Science:
- Pulmonary immunology
- Anesthesiology
- Surgical complications
Background:
- Smoking is a major risk factor for postoperative pulmonary complications.
- Alveolar macrophage function is altered by smoking.
- The impact of smoking on immune responses during anesthesia is not fully understood.
Purpose of the Study:
- To test the hypothesis that smoking impairs antimicrobial and proinflammatory responses in alveolar macrophages during anesthesia and surgery.
- To investigate the effect of smoking on macrophage function and cytokine expression in patients undergoing surgery.
Main Methods:
- Studied 30 smokers and 30 nonsmokers under propofol-fentanyl general anesthesia.
- Harvested alveolar immune cells via bronchoalveolar lavage at multiple time points.
- Measured phagocytosis, microbicidal activity, and gene expression of key proinflammatory cytokines (IL-1β, IL-6, IL-8, IFN-γ, TNF-α).
Main Results:
- Macrophage aggregation increased over time in both groups, but phagocytosis and microbicidal activity decreased significantly more in smokers.
- Gene expression of most proinflammatory cytokines increased in both groups, but less so in smokers for IL-1β, IFN-γ, and TNF-α.
- Smokers exhibited nearly twice the reduction in phagocytic and microbicidal activity compared to nonsmokers.
Conclusions:
- Smoking is associated with impaired alveolar macrophage phagocytic and microbicidal activity post-anesthesia and surgery.
- Reduced expression of proinflammatory cytokines in smokers may contribute to impaired pulmonary immune defense.
- Smokers may have a limited ability to mount an effective pulmonary immune response after anesthesia and surgery.