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Abstract: Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.
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Citation: Walters DM, Breysse PN, Schofield B, Wills-Karp M. Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness. American Journal of Respiratory Cell and Molecular Biology 2002;27(4):413-418.
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.
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