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(Journal of Leukocyte Biology. 2001;70:610-616.)
© 2001 by Society for Leukocyte Biology

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

Annie Pardo*, Kathleen M. Smith{dagger}, John Abrams{dagger}, Robert Coffman{dagger}, Martha Bustos*, Terrill K. McClanahan{dagger}, Jeffrey Grein{dagger}, Erin E. Murphy{dagger}, Albert Zlotnik{dagger} and Moisés Selman{ddagger}

* Facultad de Ciencias, Universidad Nacional Autónoma de México, and
{ddagger} Instituto Nacional de Enfermedades Respiratorias, México City, Mexico; and
{dagger} DNAX Research Institute, Palo Alto, California 94304

Correspondence: Moisés Selman, M.D., Instituto Nacional de Enfermedades Respiratorias Tlalpan 4502, Col. Sección XVI México DF, CP 14080, Mexico. E-mail: mselman{at}conacyt.mx

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.

Key Words: chemokines • T lymphocytes • cell trafficking • allergic alveolitis




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