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Asthma exacerbations · 3: Pathogenesis
  1. P A B Wark,
  2. P G Gibson
  1. Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, University of Newcastle, and John Hunter Hospital, Newcastle, NSW 2310, Australia
  1. Correspondence to:
    Professor P G Gibson
    Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, Locked Bag 1, Hunter Region Mail Centre, NSW 2310 Australia; Peter.Gibson{at}hnehealth.nsw.gov.au

Abstract

Asthma exacerbations are an exaggerated lower airway response to an environmental exposure. Respiratory virus infection is the most common environmental exposure to cause a severe asthma exacerbation. Airway inflammation is a key part of the lower airway response in asthma exacerbation, and occurs together with airflow obstruction and increased airway responsiveness. The patterns of airway inflammation differ according to the trigger factor responsible for the exacerbation. The reasons for the exaggerated response of asthmatic airways are not completely understood, but recent studies have identified a deficient epithelial type 1 interferon response as an important susceptibility mechanism for viral infection.

  • BEC, bronchial epithelial cell
  • ECP, eosinophil cationic protein
  • FEV1, forced expiratory volume in 1 second
  • ICAM-1, intercellular adhesion molecule 1
  • IFN, interferon
  • IL, interleukin
  • LDH, lactate dehydrogenase
  • PBMC, peripheral blood monocyte
  • RV, rhinovirus
  • TNF, tumour necrosis factor
  • URTI, upper respiratory tract infection
  • asthma
  • exacerbation
  • environmental exposure
  • respiratory virus
  • pathogenesis
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Footnotes

  • Supported by NHMRC Australia, Hunter Medical Research Institute, and New South Wales Health.

  • Competing interests: The authors have participated in clinical trials of asthma therapies funded by GlaxoSmithKline, AstraZeneca, Pharmaxis, Aventis, Novartis and NHMRC Australia.

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