| Summary: | <p>Abstract</p> <p>Background</p> <p>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<sup>+ </sup>T cells accumulate in pediatric ILD and are related to disease severity.</p> <p>Methods</p> <p>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<sup>+</sup>, CCR4<sup>+</sup>, CCR3<sup>+</sup>, CCR5<sup>+ </sup>and CXCR3<sup>+ </sup>T cells were quantified by flow-cytometry.</p> <p>Results</p> <p>CCR2<sup>+ </sup>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<sup>+ </sup>T cells in bronchoalveolar lavage fluid compared to non-fibrotic children.</p> <p>Conclusion</p> <p>The results indicate that pulmonary CCR2<sup>+ </sup>T cells and MCP-1 contribute to the pathogenesis of pediatric ILD and might provide a novel target for therapeutic strategies.</p>
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