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Article: Adiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in mice

TitleAdiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in mice
Authors
Issue Date2006
PublisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/jaci
Citation
Journal Of Allergy And Clinical Immunology, 2006, v. 118 n. 2, p. 389-395 How to Cite?
AbstractBackground: Epidemiologic data indicate an increased incidence of asthma in the obese. Objective: Because serum levels of the insulin-sensitizing and anti-inflammatory adipokine adiponectin are reduced in obese individuals, we sought to determine whether exogenous adiponectin can attenuate allergic airway responses. Methods: We sensitized and challenged BALB/cJ mice with ovalbumin (OVA). Alzet micro-osmotic pumps were implanted in the mice to deliver continuous infusions of buffer or adiponectin (1.0 μg/g/d), which resulted in an approximate 60% increase in serum adiponectin levels. Two days later, mice were challenged with aerosolized saline or OVA once per day for 3 days. Mice were examined 24 hours after the last challenge. Results: OVA challenge increased airway responsiveness to intravenous methacholine, bronchoalveolar lavage fluid cells, and T H2 cytokine levels. Importantly, each of these responses to OVA was reduced in adiponectin- versus buffer-treated mice. OVA challenge caused a 30% reduction in serum adiponectin levels and a corresponding decrease in adipose tissue adiponectin mRNA expression. OVA challenge also decreased pulmonary mRNA expression of each of 3 proposed adiponectin-binding proteins, adiponectin receptor 1, adiponectin receptor 2, and T-cadherin. Conclusion: Our results indicate that serum adiponectin is reduced during pulmonary allergic reactions and that adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice. Clinical implications: The data suggest that adiponectin might play a role in the relationship between obesity and asthma. © 2006 American Academy of Allergy, Asthma and Immunology.
Persistent Identifierhttp://hdl.handle.net/10722/78179
ISSN
2015 Impact Factor: 12.485
2015 SCImago Journal Rankings: 5.513
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShore, SAen_HK
dc.contributor.authorTerry, RDen_HK
dc.contributor.authorFlynt, Len_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorHug, Cen_HK
dc.date.accessioned2010-09-06T07:40:02Z-
dc.date.available2010-09-06T07:40:02Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Allergy And Clinical Immunology, 2006, v. 118 n. 2, p. 389-395en_HK
dc.identifier.issn0091-6749en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78179-
dc.description.abstractBackground: Epidemiologic data indicate an increased incidence of asthma in the obese. Objective: Because serum levels of the insulin-sensitizing and anti-inflammatory adipokine adiponectin are reduced in obese individuals, we sought to determine whether exogenous adiponectin can attenuate allergic airway responses. Methods: We sensitized and challenged BALB/cJ mice with ovalbumin (OVA). Alzet micro-osmotic pumps were implanted in the mice to deliver continuous infusions of buffer or adiponectin (1.0 μg/g/d), which resulted in an approximate 60% increase in serum adiponectin levels. Two days later, mice were challenged with aerosolized saline or OVA once per day for 3 days. Mice were examined 24 hours after the last challenge. Results: OVA challenge increased airway responsiveness to intravenous methacholine, bronchoalveolar lavage fluid cells, and T H2 cytokine levels. Importantly, each of these responses to OVA was reduced in adiponectin- versus buffer-treated mice. OVA challenge caused a 30% reduction in serum adiponectin levels and a corresponding decrease in adipose tissue adiponectin mRNA expression. OVA challenge also decreased pulmonary mRNA expression of each of 3 proposed adiponectin-binding proteins, adiponectin receptor 1, adiponectin receptor 2, and T-cadherin. Conclusion: Our results indicate that serum adiponectin is reduced during pulmonary allergic reactions and that adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice. Clinical implications: The data suggest that adiponectin might play a role in the relationship between obesity and asthma. © 2006 American Academy of Allergy, Asthma and Immunology.en_HK
dc.languageengen_HK
dc.publisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/jacien_HK
dc.relation.ispartofJournal of Allergy and Clinical Immunologyen_HK
dc.rightsJournal of Allergy and Clinical Immunology. Copyright © Mosby, Inc.en_HK
dc.subject.meshAdiponectin - blood - genetics - pharmacologyen_HK
dc.subject.meshAdipose Tissue - drug effects - metabolismen_HK
dc.subject.meshAllergens - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBronchial Hyperreactivity - immunology - prevention & controlen_HK
dc.subject.meshBronchoalveolar Lavage Fluid - cytology - immunologyen_HK
dc.subject.meshCadherins - genetics - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation - drug effectsen_HK
dc.subject.meshImmunoglobulin E - blooden_HK
dc.subject.meshLeukocytes - drug effectsen_HK
dc.subject.meshLung - drug effects - physiologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshOvalbumin - pharmacologyen_HK
dc.subject.meshPneumonia - immunology - prevention & controlen_HK
dc.subject.meshRNA, Messenger - biosynthesisen_HK
dc.subject.meshReceptors, Adiponectinen_HK
dc.subject.meshReceptors, Cell Surface - genetics - metabolismen_HK
dc.subject.meshRecombinant Proteins - pharmacologyen_HK
dc.titleAdiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0091-6749&volume=118&spage=389&epage=95&date=2006&atitle=Adiponectin+attenuates+allergen-induced+airway+inflammation+and+hyperresponsiveness+in+miceen_HK
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jaci.2006.04.021en_HK
dc.identifier.pmid16890763-
dc.identifier.scopuseid_2-s2.0-33746516349en_HK
dc.identifier.hkuros123597en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33746516349&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume118en_HK
dc.identifier.issue2en_HK
dc.identifier.spage389en_HK
dc.identifier.epage395en_HK
dc.identifier.isiWOS:000239877700014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShore, SA=7101884379en_HK
dc.identifier.scopusauthoridTerry, RD=13409393000en_HK
dc.identifier.scopusauthoridFlynt, L=6506480282en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridHug, C=7004680303en_HK

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