Document Detail


New insights into pathogenesis of exercise-induced bronchoconstriction.
MedLine Citation:
PMID:  22157157     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Teal S Hallstrand
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Current opinion in allergy and clinical immunology     Volume:  12     ISSN:  1473-6322     ISO Abbreviation:  Curr Opin Allergy Clin Immunol     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-01-05     Completed Date:  2012-07-03     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  100936359     Medline TA:  Curr Opin Allergy Clin Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  42-8     Citation Subset:  IM    
Affiliation:
Department of Medicine, Division of Pulmonary and Critical Care, University of Washington, Seattle, Washington 98195, USA. tealh@uw.edu
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MeSH Terms
Descriptor/Qualifier:
Asthma, Exercise-Induced / enzymology,  immunology*
Bronchial Hyperreactivity / enzymology,  immunology*
Cysteine / immunology*
Eosinophils / immunology*
Humans
Leukotrienes / immunology*
Longitudinal Studies
Phospholipases A2 / immunology*
Grant Support
ID/Acronym/Agency:
HL089215/HL/NHLBI NIH HHS; R01 HL089215-04/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Leukotrienes; 0/cysteinyl-leukotriene; 52-90-4/Cysteine; EC 3.1.1.4/Phospholipases A2
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