Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-7-3
pubmed:abstractText
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 (10.8 x 10(3).mL(-1) versus 1.0 x 10(3).mL(-1) and 1.7 x 10(3).mL(-1) versus 0.2 x 10(3).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-gamma 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0903-1936
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
59-67
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
CC chemokine ligand 1 is released into the airways of atopic asthmatics.
pubmed:affiliation
Dept of Immunogenetics and Allergy, National Institute of Respiratory Diseases, Calzada Tlalpan 4502, C.P. 14080, Mexico City, Mexico.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't