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2010-07-08Zeitschriftenartikel DOI: 10.1186/1465-9921-11-93
Legionella pneumophila induces human beta Defensin-3 in pulmonary cells
dc.contributor.authorScharf, Stefanie
dc.contributor.authorVardarova, Kremena
dc.contributor.authorLang, Friederike
dc.contributor.authorSchmeck, Bernd
dc.contributor.authorOpitz, Bastian
dc.contributor.authorFlieger, Antje
dc.contributor.authorHeuner, Klaus
dc.contributor.authorHippenstiel, Stefan
dc.contributor.authorSuttorp, Norbert
dc.contributor.authorN'Guessan, Philippe D
dc.date.accessioned2018-05-07T14:01:57Z
dc.date.available2018-05-07T14:01:57Z
dc.date.created2010-07-27
dc.date.issued2010-07-08none
dc.identifier.otherhttp://edoc.rki.de/oa/articles/reHPVfX3KA8vM/PDF/21D1t3iFtYkMU.pdf
dc.identifier.urihttp://edoc.rki.de/176904/690
dc.description.abstractBackground: Legionella pneumophila is an important causative agent of severe pneumonia in humans. Human alveolar epithelium and macrophages are effective barriers for inhaled microorganisms and actively participate in the initiation of innate host defense. The beta defensin-3 (hBD-3), an antimicrobial peptide is an important component of the innate immune response of the human lung. Therefore we hypothesize that hBD-3 might be important for immune defense towards L. pneumophila. Methods: We investigated the effects of L. pneumophila and different TLR agonists on pulmonary cells in regard to hBD-3 expression by ELISA. Furthermore, siRNA-mediated inhibition of TLRs as well as chemical inhibition of potential downstream signaling molecules was used for functional analysis. Results: L. pneumophila induced release of hBD-3 in pulmonary epithelium and alveolar macrophages. A similar response was observed when epithelial cells were treated with different TLR agonists. Inhibition of TLR2, TLR5, and TLR9 expression led to a decreased hBD-3 expression. Furthermore expression of hBD-3 was mediated through a JNK dependent activation of AP-1 (c-Jun) but appeared to be independent of NF-κB. Additionally, we demonstrate that hBD-3 elicited a strong antimicrobial effect on L. pneumophila replication. Conclusions: Taken together, human pulmonary cells produce hBD-3 upon L. pneumophila infection via a TLR-JNK-AP- 1-dependent pathway which may contribute to an efficient innate immune defense.eng
dc.language.isoeng
dc.publisherRobert Koch-Institut
dc.subjectHumanseng
dc.subjectCulturedeng
dc.subjectTime Factorseng
dc.subjectEpithelial Cells/microbiologyeng
dc.subjectLegionella pneumophila/immunologyeng
dc.subjectNF-kappa B/metabolismeng
dc.subjectTranscription Factor AP-1/metabolismeng
dc.subjectLegionella pneumophila/growth & developmenteng
dc.subjectRecombinant Proteins/metabolismeng
dc.subjectCellseng
dc.subjectEpithelial Cells/immunologyeng
dc.subjectEpithelial Cells/metabolismeng
dc.subjectImmunityeng
dc.subjectInnateeng
dc.subjectLegionella pneumophila/pathogenicityeng
dc.subjectMAP Kinase Kinase 4/metabolismeng
dc.subjectMacrophageseng
dc.subjectAlveolar/immunologyeng
dc.subjectAlveolar/metabolismeng
dc.subjectAlveolar/microbiologyeng
dc.subjectRespiratory Mucosa/immunologyeng
dc.subjectRespiratory Mucosa/metabolismeng
dc.subjectRespiratory Mucosa/microbiologyeng
dc.subjectSignal Transductioneng
dc.subjectToll-Like Receptors/metabolismeng
dc.subjectUp-Regulationeng
dc.subjectbeta-Defensins/metabolismeng
dc.subject.ddc610 Medizin
dc.titleLegionella pneumophila induces human beta Defensin-3 in pulmonary cells
dc.typeperiodicalPart
dc.identifier.urnurn:nbn:de:0257-1009655
dc.identifier.doi10.1186/1465-9921-11-93
dc.identifier.doihttp://dx.doi.org/10.25646/615
local.edoc.container-titleRespiratory Research
local.edoc.fp-subtypeArtikel
local.edoc.type-nameZeitschriftenartikel
local.edoc.container-typeperiodical
local.edoc.container-type-nameZeitschrift
local.edoc.container-urlhttp://respiratory-research.com/content/11/1/93/abstract
local.edoc.container-publisher-nameBioMedCentral
local.edoc.container-volume11
local.edoc.container-issue93
local.edoc.container-year2010

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