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CCL18/DC‐CK‐1/PARC up‐regulation in hypersensitivity pneumonitis
Author(s) -
Pardo Annie,
Smith Kathleen M.,
Abrams John,
Coffman Robert,
Bustos Martha,
McClanahan Terrill K.,
Grein Jeffrey,
Murphy Erin E.,
Zlotnik Albert,
Selman Moisés
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.70.4.610
Subject(s) - ccl18 , hypersensitivity pneumonitis , bronchoalveolar lavage , chemokine , lung , immunology , dendritic cell , biology , idiopathic pulmonary fibrosis , pathogenesis , pathology , immune system , in situ hybridization , medicine , gene expression , biochemistry , gene
Hypersensitivity pneumonitis (HP) is a lung inflammatory disorder characterized by accumulation of T lymphocytes. However, the mechanisms implicated in this process remain undefined. We examined the expression of dendritic cell (DC)‐derived CC chemokine 1 (CK1)/CCL18, a chemokine putatively involved in naive T cell recruitment, in lungs from 10 patients with HP, 9 patients with idiopathic pulmonary fibrosis (IPF), and 20 healthy lungs. CCL18 was measured by real‐time quantitative PCR and localized in lungs by in situ hybridization and immunohistochemistry. CCL18 expression was significantly increased in lungs affected by HP in comparison with lungs affected by IPF (2,085±393 vs. 1,023±110; P <0.05) and controls (2,085±393 vs. 467±94; P <0.01). Macrophages, DCs, and alveolar epithelial cells were the main sources of CCL18. There was a direct correlation between the levels of tissue CCL18 and the number of lymphocytes in the bronchoalveolar lavage fluids. High levels of CCL18 were detected in the subacute rather than the chronic phase of HP. These findings suggest a role for CCL18 in the pathogenesis of HP.