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Curr Opin Allergy Clin Immunol. 2012 Feb;12(1):42-8. doi: 10.1097/ACI.0b013e32834ecc67.

New insights into pathogenesis of exercise-induced bronchoconstriction.

Author information

1
Department of Medicine, Division of Pulmonary and Critical Care, University of Washington, Seattle, Washington 98195, USA. tealh@uw.edu

Abstract

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 A(2) (sPLA(2)) 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 A(2) group X (sPLA(2)-X). Further, sPLA(2)-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.

PMID:
22157157
PMCID:
PMC3289409
DOI:
10.1097/ACI.0b013e32834ecc67
[Indexed for MEDLINE]
Free PMC Article
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