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New insights into pathogenesis of exercise-induced bronchoconstriction

Hallstrand, Teal S.

Current Opinion in Allergy and Clinical Immunology: February 2012 - Volume 12 - Issue 1 - p 42–48
doi: 10.1097/ACI.0b013e32834ecc67
MECHANISMS OF ALLERGY AND ADULT ASTHMA: Edited by Stephen T. Holgate and J. Andrew Grant

Purpose of review Exercise-induced bronchoconstriction (EIB) refers to acute airflow obstruction that is triggered by a period of physical exertion. Here we review recent findings about the epidemiology of EIB, immunopathology leading to EIB, and the latest understanding of the pathogenesis of EIB.

Recent findings Longitudinal studies demonstrated that airway hyper-responsiveness to exercise or cold air at an early age are among the strongest predictors of persistent asthma. Patients that are susceptible to EIB have epithelial disruption and increased levels of inflammatory eicosanoids such as cysteinyl leukotrienes (CysLT)s. The leukocytes implicated in production of eicosanoids in the airways include both a unique mast cell population as well as eosinophils. A secreted phospholipase A2 (sPLA2) enzyme that serves as a regulator of CysLT formation is present in increased quantities in asthma. Transglutaminase 2 (TGM2) is expressed at increased levels in asthma and serves as a regulator of secreted phospholipase A2 group X (sPLA2-X). Further, sPLA2-X acts on target cells such as eosinophils to initiate cellular eicosanoid synthesis.

Summary Recent studies have advanced our understanding of EIB as a syndrome that is caused by the increased production of inflammatory eicosanoids. The airway epithelium may be an important regulator of the production of inflammatory eicosanoids by leukocytes.

Department of Medicine, Division of Pulmonary and Critical Care, University of Washington, Seattle, Washington, USA

Correspondence to Teal S. Hallstrand, MD, MPH, Associate Professor of Medicine, University of Washington, Division of Pulmonary and Critical Care, Box 356522, 1959 NE Pacific Street, Seattle, WA 98195, USA. Tel: +1 206 543 3166; fax: +1 206 685 8673; e-mail:

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