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Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

Dianne M Walters1, Patrick N Breysse, Brian Schofield

  • 1Johns Hopkins School of Hygiene and Public Health, Baltimore, Maryland, USA.

American Journal of Respiratory Cell and Molecular Biology
|October 3, 2002
PubMed
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Particulate matter (PM) exposure can worsen allergic airway responses. Complement factor 3 (C3) plays a key role in PM-induced airway hyperresponsiveness (AHR), but not inflammation.

Area of Science:

  • Immunology
  • Environmental Health
  • Pulmonology

Background:

  • Epidemiologic studies link airborne particulate matter (PM) exposure to exacerbated allergic airway responses.
  • The precise mechanisms underlying PM-induced airway hyperresponsiveness (AHR) remain unclear.
  • Recent research suggests a role for complement-mediated processes in AHR development.

Purpose of the Study:

  • To investigate the role of complement factor 3 (C3) in PM-induced AHR and airway inflammation.
  • To compare the responses of C3-deficient (C3(-/-)) mice with wild-type mice following PM exposure.

Main Methods:

  • Mice (wild-type and C3(-/-)) were exposed to ambient particulate matter.
  • Airway responsiveness to acetylcholine was assessed 48 hours post-exposure.

Related Experiment Videos

  • Bronchoalveolar lavage and immunohistochemical staining were performed to evaluate inflammation and C3 deposition.

    • Main Results:

    • PM exposure significantly increased AHR in wild-type mice but not in C3(-/-) mice.
    • PM induced comparable inflammatory responses in both wild-type and C3(-/-) mice.
    • Significant C3 deposition was observed in the airways of wild-type mice after PM exposure.

    Conclusions:

    • Complement factor 3 (C3) activation is critical for the development of PM-induced airway hyperresponsiveness (AHR).
    • PM-induced airway inflammation occurs independently of C3 activation.
    • These findings suggest C3 activation as a potential therapeutic target for mitigating PM-induced AHR.