Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness

Dianne M. Walters, Patrick N. Breysse, Brian Schofield, Marsha Wills-Karp

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)413-418
Number of pages6
JournalAmerican journal of respiratory cell and molecular biology
Volume27
Issue number4
DOIs
StatePublished - Oct 2002
Externally publishedYes

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ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology

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