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Complement activation is critical to airway hyperresponsiveness after acute ozone exposure

박중원

American Thoracic Society 2004-03

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  • Título:
    Complement activation is critical to airway hyperresponsiveness after acute ozone exposure
  • Autor: 박중원
  • Assuntos: airway hyperresponsiveness ; complement activation ; Ozone
  • Notas: https://www.krm.or.kr/krmts/link.html?dbGubun=SD&m201_id=10000938&local_id=10003653
    Am J Repir Crit Care Med, vol : 169권, issue : 0호
  • Descrição: Ozone (O3) can induce airway hyperresponsiveness and neutrophilic inflammation. We evaluated the role of complement in mice. Mice were exposed O3 at 2 ppm for 3 hours, and airway reponsiveness to methacholine was measured 8 hours after O3 exposure. Complement was depleted or inhibited by intraperitoneal injection of cobra venom factor (CVF) or complement receptor-related gene y (Crry)-Ig, a potent C3 convertase inhibitor; neutrophils were depleted using an antineutrophil monoclonal antibody. CVF attenuated the development of AHR by O3. Administration of Crry-Ig also prevented the development of AHR. Bronchoalveolar lavage (BAL) fluid neutrophilia after O3 exposure was significantly decreased by administration of either CVF or Crry-Ig. Increased BAL fluid total protein after O3 exposure was lowered by depletion or inhibition of complement. In contrast to the effects of complement inhibition or depletion, depletion of BAL neutrophil counts by more than 90% with the monoclonal antibody did not affect the development of AHR after O3 exposure. These data indicated that activation of the complement sytem follow acute O3 exposure and is important to the development of AHR and airway neutrophilia. However, this neutrophil response doe not appear necessary for the development of AHR.
  • Editor: American Thoracic Society
  • Data de criação/publicação: 2004-03
  • Idioma: Coreano
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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