Publikation:

Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA

Vorschaubild

Dateien

Zu diesem Dokument gibt es keine Dateien.

Datum

2011

Autor:innen

van Zoelen, Marieke A. D.
Verstege, Marleen I.
Draing, Christian
de Beer, Regina
van't Veer, Cornelis
Florquin, Sandrine
Bresser, Paul
Van der Zee, Jaring S.
te Velde, Anje A.
1 mehr anzeigen

Herausgeber:innen

Kontakt

ISSN der Zeitschrift

Electronic ISSN

ISBN

Bibliografische Daten

Verlag

Schriftenreihe

Auflagebezeichnung

URI (zitierfähiger Link)
DOI (zitierfähiger Link)
https://doi.org/10.1016/j.molimm.2011.04.001
ArXiv-ID

Internationale Patentnummer

Angaben zur Forschungsförderung

Projekt

Open Access-Veröffentlichung

Sammlungen

Biologie: Publikationen
Core Facility der Universität Konstanz

Gesperrt bis

Titel in einer weiteren Sprache

Publikationstyp
Zeitschriftenartikel
Publikationsstatus
Published

Erschienen in

Molecular Immunology. Elsevier. 2011, 48(12-13), pp. 1468-1476. ISSN 0161-5890. eISSN 1872-9142. Available under: doi: 10.1016/j.molimm.2011.04.001

Zusammenfassung

Monocyte chemoattractant protein 1 (MCP-1) plays an important role in leukocyte recruitment to sites of infection and inflammation. In addition, MCP-1 may attenuate inflammation by virtue of its capacity to inhibit the production of proinflammatory cytokines. We here investigated the role of MCP-1 in lung inflammation induced by lipopolysaccharide (LPS) or lipoteichoic acid (LTA), constituents of the gram-negative and gram-positive bacterial cell wall, respectively. Healthy humans demonstrated elevated MCP-1 concentrations in their bronchoalveolar lavage fluid (BALF) 6 h after inhalation of LPS. Similarly, intranasal administration of LPS or LTA to mice resulted in a rise in BALF MCP-1 levels. Murine alveolar macrophage-like cells released significant amounts of MCP-1 upon stimulation with LPS or LTA in vitro. Compared to Wt mice, MCP-1−/− mice demonstrated lower TNF-α levels and a diminished neutrophil influx into their bronchoalveolar space after either LPS or LTA instillation. After intrapulmonary delivery of LPS MCP-1−/− mice had decreased interleukin-6 and KC concentrations and less severe lung inflammation upon histopathological examination. Remarkably, MCP-1 deficiency was associated with an early enhancement of interleukin-10 release in BALF after both LPS and LTA instillation. These data suggest that MCP-1 is a proinflammatory mediator during pulmonary inflammation induced by either LPS or LTA.

Zusammenfassung in einer weiteren Sprache

Fachgebiet (DDC)
570 Biowissenschaften, Biologie

Schlagwörter

Lung inflammation; Lipopolysaccharide; Lipoteichoic acid; Monocyte chemoattractant protein 1; Soluble receptor for advanced glycation end products; Animal models

Konferenz

Rezension
undefined / . - undefined, undefined

Forschungsvorhaben

Organisationseinheiten

Zeitschriftenheft

Zugehörige Datensätze in KOPS

Zitieren

ISO 690VAN ZOELEN, Marieke A. D., Marleen I. VERSTEGE, Christian DRAING, Regina DE BEER, Cornelis VAN'T VEER, Sandrine FLORQUIN, Paul BRESSER, Jaring S. VAN DER ZEE, Anje A. TE VELDE, Sonja von AULOCK, Tom VAN DER POLL, 2011. Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA. In: Molecular Immunology. Elsevier. 2011, 48(12-13), pp. 1468-1476. ISSN 0161-5890. eISSN 1872-9142. Available under: doi: 10.1016/j.molimm.2011.04.001
BibTex
@article{vanZoelen2011-07Endog-51216,
  year={2011},
  doi={10.1016/j.molimm.2011.04.001},
  title={Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA},
  number={12-13},
  volume={48},
  issn={0161-5890},
  journal={Molecular Immunology},
  pages={1468--1476},
  author={van Zoelen, Marieke A. D. and Verstege, Marleen I. and Draing, Christian and de Beer, Regina and van't Veer, Cornelis and Florquin, Sandrine and Bresser, Paul and Van der Zee, Jaring S. and te Velde, Anje A. and Aulock, Sonja von and van der Poll, Tom}
}
RDF
<rdf:RDF
    xmlns:dcterms="http://purl.org/dc/terms/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
    xmlns:bibo="http://purl.org/ontology/bibo/"
    xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#"
    xmlns:foaf="http://xmlns.com/foaf/0.1/"
    xmlns:void="http://rdfs.org/ns/void#"
    xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > 
  <rdf:Description rdf:about="https://kops.uni-konstanz.de/server/rdf/resource/123456789/51216">
    <dc:creator>Verstege, Marleen I.</dc:creator>
    <dcterms:abstract xml:lang="eng">Monocyte chemoattractant protein 1 (MCP-1) plays an important role in leukocyte recruitment to sites of infection and inflammation. In addition, MCP-1 may attenuate inflammation by virtue of its capacity to inhibit the production of proinflammatory cytokines. We here investigated the role of MCP-1 in lung inflammation induced by lipopolysaccharide (LPS) or lipoteichoic acid (LTA), constituents of the gram-negative and gram-positive bacterial cell wall, respectively. Healthy humans demonstrated elevated MCP-1 concentrations in their bronchoalveolar lavage fluid (BALF) 6 h after inhalation of LPS. Similarly, intranasal administration of LPS or LTA to mice resulted in a rise in BALF MCP-1 levels. Murine alveolar macrophage-like cells released significant amounts of MCP-1 upon stimulation with LPS or LTA in vitro. Compared to Wt mice, MCP-1&lt;sup&gt;−/−&lt;/sup&gt; mice demonstrated lower TNF-α levels and a diminished neutrophil influx into their bronchoalveolar space after either LPS or LTA instillation. After intrapulmonary delivery of LPS MCP-1&lt;sup&gt;−/−&lt;/sup&gt; mice had decreased interleukin-6 and KC concentrations and less severe lung inflammation upon histopathological examination. Remarkably, MCP-1 deficiency was associated with an early enhancement of interleukin-10 release in BALF after both LPS and LTA instillation. These data suggest that MCP-1 is a proinflammatory mediator during pulmonary inflammation induced by either LPS or LTA.</dcterms:abstract>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dc:contributor>van Zoelen, Marieke A. D.</dc:contributor>
    <dc:contributor>de Beer, Regina</dc:contributor>
    <dc:contributor>van't Veer, Cornelis</dc:contributor>
    <dc:contributor>Florquin, Sandrine</dc:contributor>
    <dc:creator>Aulock, Sonja von</dc:creator>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dc:contributor>te Velde, Anje A.</dc:contributor>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:creator>Van der Zee, Jaring S.</dc:creator>
    <dc:creator>van Zoelen, Marieke A. D.</dc:creator>
    <dc:creator>Florquin, Sandrine</dc:creator>
    <dc:contributor>van der Poll, Tom</dc:contributor>
    <dc:contributor>Van der Zee, Jaring S.</dc:contributor>
    <dc:contributor>Verstege, Marleen I.</dc:contributor>
    <dcterms:issued>2011-07</dcterms:issued>
    <dc:creator>van der Poll, Tom</dc:creator>
    <dc:creator>van't Veer, Cornelis</dc:creator>
    <dc:creator>de Beer, Regina</dc:creator>
    <dc:language>eng</dc:language>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:creator>Draing, Christian</dc:creator>
    <dc:contributor>Bresser, Paul</dc:contributor>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-10-06T09:00:53Z</dcterms:available>
    <bibo:uri rdf:resource="https://kops.uni-konstanz.de/handle/123456789/51216"/>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-10-06T09:00:53Z</dc:date>
    <dc:contributor>Draing, Christian</dc:contributor>
    <dc:contributor>Aulock, Sonja von</dc:contributor>
    <dcterms:title>Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA</dcterms:title>
    <dc:creator>te Velde, Anje A.</dc:creator>
    <dc:creator>Bresser, Paul</dc:creator>
  </rdf:Description>
</rdf:RDF>

Interner Vermerk

xmlui.Submission.submit.DescribeStep.inputForms.label.kops_note_fromSubmitter

Kontakt
URL der Originalveröffentl.

Prüfdatum der URL

Prüfungsdatum der Dissertation

Finanzierungsart

Kommentar zur Publikation

Allianzlizenz
Corresponding Authors der Uni Konstanz vorhanden
Internationale Co-Autor:innen
Universitätsbibliographie
Ja
Begutachtet
Ja
Diese Publikation teilen