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Protective action of thiols on neutrophil function
European Journal of Respiratory Diseases. Supplement
|January 1, 1985
Summary
Cigarette smoke significantly impairs polymorphonuclear leukocyte (PMN) function, specifically their ability to move towards chemical signals (chemotaxis). Acrolein and crotonaldehyde in smoke are key inhibitors, potentially increasing smokers' susceptibility to infections.
Area of Science:
- Immunology
- Toxicology
Background:
- Smokers exhibit reduced polymorphonuclear leukocyte (PMN) chemotaxis, suggesting an acute effect of smoking.
- Understanding the specific components and mechanisms of smoke-induced PMN dysfunction is crucial.
Purpose of the Study:
- To investigate the in vitro inhibitory effects of cigarette smoke on PMN chemotaxis.
- To identify potent inhibitory fractions and components within cigarette smoke.
- To elucidate the mechanism underlying smoke-induced chemotaxis inhibition.
Main Methods:
- Exposure of PMNs to whole cigarette smoke, gas phase, and water-soluble fraction (WSF).
- Fractionation of smoke condensate based on polarity.
- Testing specific smoke constituents like acrolein and crotonaldehyde.
- Assessment of protective effects using cysteine and reduced glutathione.
Main Results:
- Whole smoke, gas phase, and WSF potently inhibited PMN chemotaxis.
- Polar fractions of smoke condensate were stronger inhibitors than nonpolar fractions.
- Acrolein and crotonaldehyde were identified as potent inhibitors.
- Cysteine offered complete protection against WSF, acrolein, and crotonaldehyde, but partial protection against whole smoke and gas phase.
- Reduced glutathione provided complete protection against WSF and partial protection against polar fractions.
Conclusions:
- Cigarette smoke, particularly its polar components like acrolein and crotonaldehyde, significantly inhibits PMN chemotaxis in vitro.
- Impaired PMN chemotaxis due to smoke exposure may contribute to increased risk of bronchopulmonary infections in smokers.