Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness

Am J Respir Cell Mol Biol. 2002 Oct;27(4):413-8. doi: 10.1165/rcmb.4844.


Epidemiologic studies have suggested that exposure to airborne particulate matter (PM) can exacerbate allergic airway responses; however, the mechanism(s) are not well understood. We and others have recently shown that development of airway hyperresponsiveness (AHR) may be a complement-mediated process. In the present study, we examined the role of complement factor 3 (C3) in the development of PM-induced AHR and airway inflammation by comparing responses between C3-deficient (C3(-/-)) and wild-type mice. Mice were exposed to 0.5 mg of ambient particulate collected in urban Baltimore. Forty-eight hours later, airway responsiveness to intravenous acetylcholine was assessed and bronchoalveolar lavage was conducted. PM exposure of wild-type mice resulted in significant increases in AHR, whereas it did not significantly increase airway reactivity in C3(-/-) mice. Interestingly, PM induced similar inflammatory responses in both wild-type and C3(-/-) mice. Immunohistochemical staining demonstrated marked C3 deposition in the airway epithelium and connective tissue of wild-type mice after PM exposure. These results suggest that exposure to PM may induce AHR through activation of complement factor 3 in the airways.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Air Pollution* / analysis
  • Animals
  • Bronchi / immunology*
  • Bronchi / metabolism*
  • Bronchoalveolar Lavage Fluid / chemistry
  • Bronchoalveolar Lavage Fluid / cytology
  • Complement C3 / metabolism*
  • Complement C3 / physiology*
  • Eosinophils / pathology
  • Epithelial Cells / pathology
  • Immunohistochemistry
  • Inflammation
  • Lung / pathology
  • Macrophages / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neutrophils / pathology


  • Complement C3