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dc.contributor.authorL. Asquith, Kelly
dc.contributor.authorC. Horvat, Jay
dc.contributor.authorE. Kaiko, Gerard
dc.contributor.authorCarey, Alison
dc.contributor.authorW. Beagley, Kenneth
dc.contributor.authorM. Hansbro, Philip
dc.contributor.authorS. Foster, Paul
dc.date.accessioned2017-05-03T15:53:03Z
dc.date.available2017-05-03T15:53:03Z
dc.date.issued2011
dc.date.modified2012-03-06T05:42:55Z
dc.identifier.issn1553-7366
dc.identifier.doi10.1371/journal.ppat.1001339
dc.identifier.urihttp://hdl.handle.net/10072/42522
dc.description.abstractChlamydiae are intracellular bacteria that commonly cause infections of the respiratory and genital tracts, which are major clinical problems. Infections are also linked to the aetiology of diseases such as asthma, emphysema and heart disease. The clinical management of infection is problematic and antibiotic resistance is emerging. Increased understanding of immune processes that are involved in both clearance and immunopathology of chlamydial infection is critical for the development of improved treatment strategies. Here, we show that IL-13 was produced in the lungs of mice rapidly after Chlamydia muridarum (Cmu) infection and promoted susceptibility to infection. Wild-type (WT) mice had increased disease severity, bacterial load and associated inflammation compared to IL-13 deficient (-/-) mice as early as 3 days post infection (p.i.). Intratracheal instillation of IL-13 enhanced bacterial load in IL-13-/- mice. There were no differences in early IFN-g and IL-10 expression between WT and IL-13-/- mice and depletion of CD4+ T cells did not affect infection in IL-13-/- mice. Collectively, these data demonstrate a lack of CD4+ T cell involvement and a novel role for IL-13 in innate responses to infection. We also showed that IL-13 deficiency increased macrophage uptake of Cmu in vitro and in vivo. Moreover, the depletion of IL-13 during infection of lung epithelial cells in vitro decreased the percentage of infected cells and reduced bacterial growth. Our results suggest that enhanced IL-13 responses in the airways, such as that found in asthmatics, may promote susceptibility to chlamydial lung infection. Importantly the role of IL-13 in regulating infection was not limited to the lung as we showed that IL-13 also promoted susceptibility to Cmu genital tract infection. Collectively our findings demonstrate that innate IL-13 release promotes infection that results in enhanced inflammation and have broad implications for the treatment of chlamydial infections and IL-13-associated diseases.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.format.extent514364 bytes
dc.format.mimetypeapplication/pdf
dc.languageEnglish
dc.language.isoeng
dc.publisherPublic Library of Science
dc.publisher.placeUnited States
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrome1001339-1
dc.relation.ispartofpagetoe1001339-10
dc.relation.ispartofissue5
dc.relation.ispartofjournalPLoS Pathogens
dc.relation.ispartofvolume7
dc.rights.retentionY
dc.subject.fieldofresearchCellular Immunology
dc.subject.fieldofresearchInfectious Agents
dc.subject.fieldofresearchMicrobiology
dc.subject.fieldofresearchImmunology
dc.subject.fieldofresearchMedical Microbiology
dc.subject.fieldofresearchcode110704
dc.subject.fieldofresearchcode060502
dc.subject.fieldofresearchcode0605
dc.subject.fieldofresearchcode1107
dc.subject.fieldofresearchcode1108
dc.titleInterleukin-13 Promotes Susceptibility to Chlamydial Infection of the Respiratory and Genital Tracts
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dcterms.licensehttp://www.plos.org/journals/license.html
gro.rights.copyright© 2011, Asquith et al. This is an Open Access article distributed under the terms of the Creative Commons Attribution License CCAL. (http://www.plos.org/journals/license.html)
gro.date.issued2011
gro.hasfulltextFull Text
gro.griffith.authorCarey, Alison


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