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Hartl, D.* ; Griese, M.* ; Nicolai, T.* ; Zissel, G.* ; Prell, C.* ; Reinhardt, D.* ; Schendel, D.J. ; Krauss-Etschmann, S.

A role for MCP-I/CCR2 in interstitial lung disease in children.

Respir. Res. 6, 93-104 (2005)
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Open Access Gold
Creative Commons Lizenzvertrag
BACKGROUND: Interstitial lung diseases (ILD) are chronic inflammatory disorders leading to pulmonary fibrosis. Monocyte chemotactic protein 1 (MCP-1) promotes collagen synthesis and deletion of the MCP-1 receptor CCR2 protects from pulmonary fibrosis in ILD mouse models. We hypothesized that pulmonary MCP-1 and CCR2+ T cells accumulate in pediatric ILD and are related to disease severity. METHODS: Bronchoalveolar lavage fluid was obtained from 25 children with ILD and 10 healthy children. Levels of pulmonary MCP-1 and Th1/Th2-associated cytokines were quantified at the protein and the mRNA levels. Pulmonary CCR2+, CCR4+, CCR3+, CCR5+ and CXCR3+ T cells were quantified by flow-cytometry. RESULTS: CCR2+ T cells and MCP-1 levels were significantly elevated in children with ILD and correlated with forced vital capacity, total lung capacity and ILD disease severity scores. Children with lung fibrosis had significantly higher MCP-1 levels and CCR2+ T cells in bronchoalveolar lavage fluid compared to non-fibrotic children. CONCLUSION: The results indicate that pulmonary CCR2+ T cells and MCP-1 contribute to the pathogenesis of pediatric ILD and might provide a novel target for therapeutic strategies.  
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2005
HGF-Berichtsjahr 0
ISSN (print) / ISBN 1465-9921
e-ISSN 1465-993X
Zeitschrift Respiratory Research
Quellenangaben Band: 6, Heft: , Seiten: 93-104 Artikelnummer: , Supplement: ,
Verlag BioMed Central
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)
POF Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er) Immune Response and Infection
PSP-Element(e) G-501700-001
DOI 10.1186/1465-9921-6-93
Erfassungsdatum 2005-09-29
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