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Impaired alveolar macrophage chemotaxis in patients with acute smoke inhalation
Abstract:
Pulmonary infection is a leading cause of death in patients with smoke inhalation; however, few studies have evaluated the effects of inhaled smoke on the host defense mechanisms of the lung. In this study we investigated the effects of acute smoke inhalation on the random and chemotactic (stimulated unidirectional) migration of human pulmonary alveolar macrophages. Fiberoptic subsegmental pulmonary lavage was performed in 19 normal subjects (12 nonsmokers and 7 smokers) and 7 patients with smoke inhalation. After quantification of lavaged cell populations, random and chemotactic migration was measured using modified Boyden chambers. Zymosan-activated serum was used as a chemotactic stimulant. Mean +/- SE random migration was 6.2 +/- 0.8 cells per 20 microscopic fields in smoking control subjects, 5.7 +/- 0.7 in nonsmoking control subjects, and 5.2 +/- 0.7 in patients with smoke inhalation. These values are not significantly different. In contrast, the mean directed (chemotactic) migration of pulmonary alveolar macrophages was 26.5 +/- 1.9 in smoking control subjects, 22.7 +/- 3.0 in nonsmoking control subjects, and 11.4 +/- 1.4 in patients with smoke inhalation; the latter response was significantly different from that of the smoking (P less than 0.001) and nonsmoking (P less than 0.025) control subjects and the combined average of the 2 control groups (P less than 0.001. In vitro exposure of pulmonary alveolar macrophages to nontoxic doses of smoke produced similar impairment of chemotaxis. These findings may partially explain the enhanced susceptibility of patients with smoke inhalation to pulmonary infection.
Insights
Smoke inhalation impairs pulmonary alveolar macrophage function, specifically their ability to migrate towards infection signals. This reduced immune cell function in smoke inhalation patients may increase their susceptibility to lung infections.
Area of Science:
- Pulmonary immunology
- Infectious disease research
Background:
- Pulmonary infections are a major cause of mortality in smoke inhalation patients.
- The impact of inhaled smoke on lung host defense mechanisms remains understudied.
Purpose of the Study:
- To investigate the effects of acute smoke inhalation on human pulmonary alveolar macrophage migration.
- To assess both random and chemotactic migration capabilities of these immune cells.
Main Methods:
- Fiberoptic subsegmental pulmonary lavage was used to collect cells from normal smokers, nonsmokers, and smoke inhalation patients.
- Modified Boyden chambers were employed to measure random and chemotactic macrophage migration.
- Zymosan-activated serum served as the chemotactic stimulant.
Main Results:
- Random migration of pulmonary alveolar macrophages showed no significant difference across control groups and smoke inhalation patients.
- Chemotactic migration was significantly impaired in patients with smoke inhalation compared to both smoking and nonsmoking controls.
- In vitro smoke exposure also demonstrated a similar impairment of macrophage chemotaxis.
Conclusions:
- Acute smoke inhalation significantly impairs the chemotactic function of pulmonary alveolar macrophages.
- This functional deficit in immune cells may contribute to the increased risk of pulmonary infections observed in smoke inhalation victims.