A role for MCP-1-CCR2 in interstitial lung disease in childrenReportar como inadecuado

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Respiratory Research

, 6:93

First Online: 11 August 2005Received: 19 April 2005Accepted: 11 August 2005


BackgroundInterstitial 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.

MethodsBronchoalveolar 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.

ResultsCCR2 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.

ConclusionThe 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.

Chemokines MCP-1 CCR2 Bronchoalveolar Lavage Children Interstitial Lung Diseases AbbreviationsBALFBronchoalveolar lavage fluid

CCCC chemokine receptor

CXCCXC chemokine receptor

FVCForced vital capacity



IPFIdiopathic pulmonary fibrosis

IPHIdiopathic pulmonary hemosiderosis

LIPLymphocytic interstitial pneumonia

MCP-1Monocyte chemotactic protein 1 CCL2

PAPPulmonary alveolar proteinosis

TGF-βTransforming growth factor β

Th1-Th2T helper cell 1-2

TLCTotal lung capacity

TNF-αTumor necrosis factor-α

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Autor: Dominik Hartl - Matthias Griese - Thomas Nicolai - Gernot Zissel - Christine Prell - Dietrich Reinhardt - Dolores J Schend

Fuente: https://link.springer.com/

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