CCL18/DC-CK-1/PARC up-regulation in hypersensitivity pneumonitis

Citation
A. Pardo et al., CCL18/DC-CK-1/PARC up-regulation in hypersensitivity pneumonitis, J LEUK BIOL, 70(4), 2001, pp. 610-616
Citations number
25
Categorie Soggetti
Immunology
Journal title
JOURNAL OF LEUKOCYTE BIOLOGY
ISSN journal
07415400 → ACNP
Volume
70
Issue
4
Year of publication
2001
Pages
610 - 616
Database
ISI
SICI code
0741-5400(200110)70:4<610:CUIHP>2.0.ZU;2-N
Abstract
Hypersensitivity pneumonitis (HP) is a lung inflammatory disorder character ized by accumulation of T lymphocytes. However, the mechanisms implicated i n this process remain undefined. We examined the expression of dendritic ce ll (DC)derived CC chemokine I (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 m easured by real-time quantitative PCR and localized in lungs by in situ hyb ridization and immunohistochemistry. CCL18 expression was significantly inc reased 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 o f 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 pathoge nesis of HP.