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CC chemokine ligand 1 is released into the airways of atopic asthmatics

¹ Dept of Immunogenetics and Allergy, National Institute of Respiratory Diseases, Mexico City, ² Medical Research Unit, Mexican Institute of Social Security, Zacatecas, Mexico.

CORRESPONDENCE: L. M. Teran, Dept of Immunogenetics and Allergy, National Institute of Respiratory Diseases, Calzada Tlalpan 4502, C.P. 14080, Mexico City, Mexico. Fax: 52 556654623. E-mail: lmteran{at}iner.gob.mx

Keywords: Asthma, bronchoalveolar lavage fluid, CC chemokine ligand/I-309, lymphocytes

Received: November 23, 2004
Accepted March 10, 2006

CC chemokine ligand (CCL)1/I-309 is a potent attractant for T-helper cell type 2 lymphocytes. The present study investigates whether this cytokine is released in the bronchoalveolar fluid (BALF) of asthmatic patients.

Measurements of CCL1 using ELISA showed that levels of this cytokine were significantly elevated in BALF from asthmatics compared with normals (median (range) 193 (120–449) pg·mL^–1 versus 30 (21–55) pg·mL^–1). Differential cell counts in BALF showed that either lymphocyte or eosinophil numbers were elevated in asthmatic compared with normal subjects (10.8x10³·mL^–1 versus 1.0x10³·mL^–1 and 1.7x10³·mL^–1 versus 0.2x10³·mL^–1, respectively). There was a trend towards a significant correlation between CCL1 levels and lymphocyte numbers in BALF. Separation of BALF using sequential CCL1 affinity column and reverse-phase high-performance liquid chromatography allowed detection of biologically active CCL1. Using immunohistochemistry, CCL1 immunoreactivity was localised predominantly to the airway epithelium.

Interestingly, there was a significant correlation between CC chemokine ligand 1 levels and epithelial cell numbers in bronchoalveolar lavage fluid and between these cells and lymphocyte numbers. Moreover, interleukin-4, interleukin-13 and interferon- stimulated primary bronchial airway epithelial cells to release CC chemokine ligand 1. These findings suggest that CC chemokine ligand 1 may play a role in lymphocyte recruitment in bronchial asthma.