The CC chemokine Ligand (CCL)-1 is released into the airways of atopic asthmatics

¹ Instituto Nacional de Enfermedades Respiratorias, México
² Instituto Mexicano del Seguro Social, México

^* To whom correspondence should be addressed. E-mail: lmteran{at}iner.gob.mx.

	Abstract

CCL1/I-309 is a potent attractant for Th2 lymphocytes. We have investigated whether this cytokine is released in the bronchoalveolar (BAL) fluid of asthmatic patients. Measurements of CCL1 by ELISA showed that levels of this cytokine were significantly elevated in BAL fluid from asthmatics compared with normals (medians 193, range 120-449 pg·ml^-1 vs 30 pg·ml^-1 range 21-55 pg·ml^-1). Differential cell counts in BAL fluid showed that either lymphocyte- or eosinophil numbers were elevated in asthmatic- compared with normal subjects (median 10.8 vs 1.0x10³·ml^-1, p<0.005 and 1.7 vs 0.2x10³·ml^-1, p<0.001, respectively). There was a trend towards a significant correlation between CCL1 levels and lymphocyte numbers in BAL fluid (r=0.4, p=0.08). Separation of BAL fluid by sequential CCL1 affinity column and reverse-phase HPLC chromatography allowed detecting biologically active CCL1. By immunohistochemistry, CCL1 immunoreactivity was localized predominantly to the airway epithelium. Interestingly, there was a significant correlation between CCL1 levels and epithelial cell numbers (r=0.73, p=0.001) in BAL fluid and between these cells and lymphocyte numbers (r=0.6, p=0.02). Moreover, IL-4, IL-13 or IFN-gamma stimulated primary bronchial airway epithelial cells to release CCL1. These findings suggest that CCL1 may play a role in lymphocyte recruitment in bronchial asthma.