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Complement activation by cigarette smoke.

R A Robbins¹, K J Nelson, G L Gossman

¹Research Service, Omaha Veterans Administration Medical Center, Nebraska.

The American Journal of Physiology

|April 1, 1991

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Cigarette smoke exposure triggers immune cell attraction in the lungs, suggesting a role for complement activation in smoking-related lung disease. This research highlights how smoke can activate the complement system, drawing neutrophils and monocytes to the lower respiratory tract.

Area of Science:

Immunology
Pulmonology
Toxicology

Background:

Lung disease from smoking involves neutrophil and monocyte influx.
The mechanism by which cigarette smoke attracts these cells is not fully understood.

Purpose of the Study:

To investigate if cigarette smoke generates chemotactic activity for neutrophils and monocytes.
To determine if cigarette smoke activates the complement system.

Main Methods:

Human serum exposed to cigarette smoke or air.
Chemotactic activity assays for neutrophils and monocytes.
Complement activation markers assessed via immunoelectrophoresis and radioimmunoassay.

Main Results:

Smoke-exposed serum showed significantly higher neutrophil and monocyte chemotaxis.

Related Experiment Videos

Complement activation suggested by partial attenuation with EDTA and observed cleavage of properdin factor B and C3.

C5a detected in smoke-exposed serum.

Conclusions:

Cigarette smoke generates chemotactic activity for neutrophils and monocytes.
Complement activation, particularly the alternate pathway, is implicated in this process.
Complement activation may contribute to the inflammatory cell influx in smokers' lungs.