CC chemokine receptor 5 (CCR5) mRNA expression in pulmonary sarcoidosis
Language English Country Netherlands Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
11803051
DOI
10.1016/s0165-2478(01)00324-8
PII: S0165247801003248
Knihovny.cz E-resources
- MeSH
- Bronchoalveolar Lavage Fluid cytology MeSH
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- RNA, Messenger genetics metabolism MeSH
- Sarcoidosis, Pulmonary genetics MeSH
- Reverse Transcriptase Polymerase Chain Reaction MeSH
- Polymorphism, Genetic genetics MeSH
- Receptors, CCR5 genetics MeSH
- Gene Expression Regulation * MeSH
- Aged MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- RNA, Messenger MeSH
- Receptors, CCR5 MeSH
The CC chemokine receptor 5 (CCR5) binds the chemokine ligands RANTES (CCL5) and MIP-1alpha (CCL3), which have been implicated in the development of alveolitis in sarcoidosis. We have, therefore, investigated CCR5 mRNA expression in bronchoalveolar lavage fluid (BALF) cells from patients with sarcoidosis. Further, we explored whether there was any association between CCR5 mRNA expression and the presence of the CCR5Delta32 DNA polymorphism. Semiquantitative RT-PCR was used to determine CCR5 mRNA expression from BALF cells from 16 control subjects (C) and 39 patients with sarcoidosis (S). The data on the CCR5Delta32 polymorphism, determined by PCR-SSP, were available for 37 patients. CCR5 mRNA expression was significantly upregulated in sarcoidosis (median+/-SEM, C, 0.00+/-0.07; S, 0.12+/-0.07; P<0.05). When patients were evaluated according to their CCR5Delta32 genotype, an interesting trend emerged with Delta32 positive patients (wt, mt) expressing less mRNA than the patients with both wild-type alleles (wt, wt): 0.00+/-0.09, and 0.26+/-0.09, respectively; P>0.05). In conclusion, upregulation of CCR5 mRNA in BALF of patients with sarcoidosis is consistent with its chemokine ligands RANTES and MIP-1alpha playing a pivotal role in inflammatory cell recruitment to disease sites. Though the data from this pilot study had no clinical correlations we suggest that further studies are warranted on the role of this Th1 subset marker in the pathogenesis of sarcoidosis.
References provided by Crossref.org
Next-Generation Sequencing Based HLA Typing: Deciphering Immunogenetic Aspects of Sarcoidosis
Expression Profile of Six RNA-Binding Proteins in Pulmonary Sarcoidosis
In vitro pharmacoregulation of CC chemokine ligand 5 and its receptor CCR5 in diffuse lung diseases