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dc.contributor.authorYang, Ming
dc.contributor.authorRangasamy, Danny
dc.contributor.authorI. Matthaei, Klaus
dc.contributor.authorJ. Frew, Ailsa
dc.contributor.authorZimmmermann, Nives
dc.contributor.authorMahalingam, Suresh
dc.contributor.authorC. Webb, Dianne
dc.contributor.authorJ. Tremethick, David
dc.contributor.authorJ. Thompson, Philip
dc.contributor.authorP. Hogan, Simon
dc.contributor.authorE. Rothenberg, Marc
dc.contributor.authorB. Cowden, William
dc.contributor.authorS. Foster, Paul
dc.date.accessioned2017-05-03T14:55:01Z
dc.date.available2017-05-03T14:55:01Z
dc.date.issued2006
dc.date.modified2013-12-12T03:46:49Z
dc.identifier.issn00221767
dc.identifier.doi10.4049/jimmunol.177.8.5595
dc.identifier.urihttp://hdl.handle.net/10072/54932
dc.description.abstractIncreased arginase I activity is associated with allergic disorders such as asthma. How arginase I contributes to and is regulated by allergic inflammatory processes remains unknown. CD4+ Th2 lymphocytes (Th2 cells) and IL-13 are two crucial immune regulators that use STAT6-dependent pathways to induce allergic airways inflammation and enhanced airways responsiveness to spasmogens (airways hyperresponsiveness (AHR)). This pathway is also used to activate arginase I in isolated cells and in hepatic infection with helminths. In the present study, we show that arginase I expression is also regulated in the lung in a STAT6-dependent manner by Th2-induced allergic inflammation or by IL-13 alone. IL-13-induced expression of arginase I correlated directly with increased synthesis of urea and with reduced synthesis of NO. Expression of arginase I, but not eosinophilia or mucus hypersecretion, temporally correlated with the development, persistence, and resolution of IL-13-induced AHR. Pharmacological supplementation with L-arginine or with NO donors amplified or attenuated IL-13-induced AHR, respectively. Moreover, inducing loss of function of arginase I specifically in the lung by using RNA interference abrogated the development of IL-13-induced AHR. These data suggest an important role for metabolism of L-arginine by arginase I in the modulation of IL-13-induced AHR and identify a potential pathway distal to cytokine receptor interactions for the control of IL-13-mediated bronchoconstriction in asthma.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherAmerican Association of Immunologists
dc.publisher.placeUnited States
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom5595
dc.relation.ispartofpageto5603
dc.relation.ispartofissue8
dc.relation.ispartofjournalJournal of Immunology
dc.relation.ispartofvolume177
dc.rights.retentionY
dc.subject.fieldofresearchImmunology not elsewhere classified
dc.subject.fieldofresearchImmunology
dc.subject.fieldofresearchcode110799
dc.subject.fieldofresearchcode1107
dc.titleInhibition of Arginase I Activity by RNA Interference Attenuates IL-13-Induced Airways Hyperresponsiveness
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.
gro.date.issued2006
gro.hasfulltextNo Full Text
gro.griffith.authorMahalingam, Suresh


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