Document Detail


Critical roles for interleukin-4 and interleukin-5 during respiratory syncytial virus infection in the development of airway hyperresponsiveness after airway sensitization.
MedLine Citation:
PMID:  10934057     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In mice, respiratory syncytial virus (RSV) infection can enhance the consequences of allergic airway sensitization, resulting in lung eosinophilia and the development of airway hyperresponsiveness (AHR) to inhaled methacholine (MCh). To delineate a role for interleukin-5 (IL-5), interleukin-4 (IL-4), and interferon gamma (IFN-gamma) in mediating the effects of RSV infection on subsequent allergic sensitization, we treated BALB/c mice with anti-IL-5 during acute RSV infection but not during subsequent exposure to ovalbumin (OVA). IL-5-deficient and IL-4-deficient mice were also treated with IL-5 either during acute RSV infection or during the sensitization period. Airway responsiveness to inhaled MCh was assessed and numbers of lung eosinophils were monitored. Anti-IL-5 treatment during RSV infection reduced AHR and lung eosinophilia after subsequent exposure to allergen. In IL-5-deficient or IL-4-deficient mice lung eosinophilia and AHR after RSV infection and allergen exposure were also markedly reduced. IL-5 administration during RSV infection restored the responses to allergen in both IL-5- and IL-4-deficient mice. However, IL-5 administration only during sensitization restored these responses in IL-4-deficient but not in IL-5-deficient animals. IFN-gamma-deficient mice developed AHR and some lung eosinophilia after allergen exposure alone and when RSV infection preceded allergen, these responses were enhanced. We conclude that both IL-5, particularly during acute infection, and IL-4 are critical in mediating the effects of RSV infection on allergic airway sensitization, resulting in the development of AHR and lung eosinophilia.
Authors:
J Schwarze; G Cieslewicz; A Joetham; T Ikemura; M J Mäkelä; A Dakhama; L D Shultz; M C Lamers; E W Gelfand
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  162     ISSN:  1073-449X     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  2000 Aug 
Date Detail:
Created Date:  2000-09-15     Completed Date:  2000-09-15     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  380-6     Citation Subset:  AIM; IM    
Affiliation:
Division of Basic Sciences, Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Female
Immunization
Interferon-gamma / physiology
Interleukin-4 / pharmacology,  physiology*
Interleukin-5 / pharmacology,  physiology*
Methacholine Chloride
Mice
Mice, Inbred BALB C
Ovalbumin / immunology
Pulmonary Eosinophilia / etiology
Respiratory Hypersensitivity / etiology*
Respiratory Syncytial Virus Infections / etiology*,  physiopathology
Grant Support
ID/Acronym/Agency:
AI-30389/AI/NIAID NIH HHS; HL-36577/HL/NHLBI NIH HHS; HL-61005/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Interleukin-5; 207137-56-2/Interleukin-4; 62-51-1/Methacholine Chloride; 82115-62-6/Interferon-gamma; 9006-59-1/Ovalbumin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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