Complement activation by cigarette smoke

R. A. Robbins, K. J. Nelson, G. L. Gossman, S. Koyama, S. I. Rennard

Research output: Contribution to journalArticlepeer-review

67 Scopus citations


Lung disease secondary to cigarette smoking is associated with an influx of neutrophils and monocytes into the lower respiratory tract. To determine whether cigarette smoke can generate chemotactic activity, human serum was exposed to cigarette smoke and evaluated for neutrophil and monocyte chemotactic activity. Serum exposed to cigarette smoke attracted significantly greater numbers of neutrophils and monocytes compared with normal human serum exposed to air (P < 0.01, both comparisons). The increase in chemotactic activity was partially attenuated by EDTA but not by ethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) and MgCl2 (P > 0.05, both comparisons), suggesting activation of the alternate complement pathway. To evaluate the capacity of cigarette smoke to activate the complement system, smoke-exposed serum was evaluated for cleavage of properdin factor B and C3 using immunoelectrophoresis and for C5a using a radioimmunoassay. Cleavage of properdin factor B and C3 was observed in the smoke-exposed serum and C5a was detected in the smoke-exposed serum (112 ± 31 ng/ml). These data suggest that complement activation may play a role in directing the influx of neutrophils and monocytes into the lungs of cigarette smokers.

Original languageEnglish (US)
Pages (from-to)L254-L259
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number4 4-2
StatePublished - 1991
Externally publishedYes


  • Complement C5a
  • Monocyte chemotaxis
  • Neutrophil chemotaxis

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


Dive into the research topics of 'Complement activation by cigarette smoke'. Together they form a unique fingerprint.

Cite this