Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-11-18
pubmed:abstractText
We have tested the hypothesis that the CysLT(1) receptor is expressed by a variety of bronchial mucosal immune cells and that the numbers of these cells increase in asthma, when stable and in exacerbations. We have applied in situ hybridization and immunohistochemistry to endobronchial biopsy tissue to identify and count inflammatory cells expressing CysLT(1) receptor mRNA and protein, respectively, and used double immunohistochemistry to identify the specific cell immunophenotypes expressing the receptor. Double-labeling demonstrated that bronchial mucosal eosinophils, neutrophils, mast cells, macrophages, B-lymphocytes, and plasma cells, but not T-lymphocytes, expressed the CysLT(1) receptor. The numbers of CysLT(1) receptor mRNA and protein positive inflammatory cells in nonsmoking, nonatopic control subjects without asthma were 13 and 16 mm(-2), respectively (median values; n = 15), and were significantly greater in stable asthma (50 and 43 mm(-2), respectively; n = 17; P < 0.001). Compared with stable asthma, there were further significant increases in subjects hospitalized for a severe exacerbation of their asthma (mRNA: median = 113 and protein: 156 mm(-2); n = 15; P < 0.002). For the combined data of both asthma subgroups, there were strong positive correlations between the increased numbers of CD45+ leukocytes and the greater numbers of cells expressing CysLT(1) receptor (mRNA: r = 0.60, P < 0.001; protein: r = 0.73, P < 0.0001). In conclusion, a variety of immunohistologically distinct inflammatory cells express the CysLT(1) receptor in the bronchial mucosa and both these and the total number of leukocytes increase in mild stable disease and increase further when there is a severe exacerbation of asthma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
531-40
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16123393-Adult, pubmed-meshheading:16123393-Aged, pubmed-meshheading:16123393-Asthma, pubmed-meshheading:16123393-B-Lymphocytes, pubmed-meshheading:16123393-Biopsy, pubmed-meshheading:16123393-Bronchi, pubmed-meshheading:16123393-Eosinophils, pubmed-meshheading:16123393-Female, pubmed-meshheading:16123393-Forced Expiratory Volume, pubmed-meshheading:16123393-Humans, pubmed-meshheading:16123393-Immunoenzyme Techniques, pubmed-meshheading:16123393-Immunophenotyping, pubmed-meshheading:16123393-In Situ Hybridization, pubmed-meshheading:16123393-Leukocytes, pubmed-meshheading:16123393-Macrophages, pubmed-meshheading:16123393-Male, pubmed-meshheading:16123393-Mast Cells, pubmed-meshheading:16123393-Membrane Proteins, pubmed-meshheading:16123393-Middle Aged, pubmed-meshheading:16123393-Mucous Membrane, pubmed-meshheading:16123393-Neutrophils, pubmed-meshheading:16123393-Plasma Cells, pubmed-meshheading:16123393-RNA, Messenger, pubmed-meshheading:16123393-RNA Probes, pubmed-meshheading:16123393-Receptors, Leukotriene, pubmed-meshheading:16123393-T-Lymphocytes, pubmed-meshheading:16123393-Up-Regulation
pubmed:year
2005
pubmed:articleTitle
Localization and upregulation of cysteinyl leukotriene-1 receptor in asthmatic bronchial mucosa.
pubmed:affiliation
Lung Pathology, Imperial College London, Royal Brompton Hospital, Sydney Street, London SW3 6NP, United Kingdom.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't