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Expression of CCX CKR in pulmonary sarcoidosis
E Kriegova, A Tsyrulnyk, A Arakelyan, F Mrazek, M Ordeltova, S Petzmann, J Zatloukal, V Kolek, Bois RM du, H Popper, M Petrek
Language English Country Switzerland
Document type Research Support, Non-U.S. Gov't
Grant support
NR9037
MZ0
CEP Register
Digital library NLK
Full text - Část
Source
NLK
ProQuest Central
from 2002-01-01 to 1 year ago
Health & Medicine (ProQuest)
from 2002-01-01 to 1 year ago
- MeSH
- Bronchoalveolar Lavage Fluid * cytology chemistry MeSH
- Middle Aged MeSH
- Humans MeSH
- RNA, Messenger biosynthesis MeSH
- Sarcoidosis, Pulmonary immunology metabolism MeSH
- Leukocyte Count MeSH
- Receptors, CCR MeSH
- Receptors, Chemokine * biosynthesis genetics MeSH
- Up-Regulation MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
OBJECTIVE: CCX CKR is a decoy chemokine receptor that specifically binds the chemokines CCL19, CCL25 and CCL21. CCL19 was previously found to be upregulated in pulmonary sarcoidosis. We have, therefore, investigated CCX CKR expression in this inflammatory disease. METHODS AND RESULTS: CCX CKR mRNA was semiquantitated using RT-PCR in unseparated bronchoalveolar (BAL) cells from sarcoidosis patients (S, n = 29) and healthy control subjects (C, n = 9). CCX CKR transcripts were upregulated in patients (mean +/- SEM); S, 0.82 +/- 0.10; C, 0.44 +/- 0.04; p = 0.01; this upregulation paralleled the disease course as assessed by the chest radiographic stage (p < 0.02). Immunocytochemistry localised the CCX CKR protein to ciliated bronchial cells. Flow cytometric fluorescent ligand uptake assay showed that these cells are able to internalize its ligand. CONCLUSION: These observations implicate CCX CKR in the modulation of the inflammatory response in sarcoidosis.
References provided by Crossref.org
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- $a OBJECTIVE: CCX CKR is a decoy chemokine receptor that specifically binds the chemokines CCL19, CCL25 and CCL21. CCL19 was previously found to be upregulated in pulmonary sarcoidosis. We have, therefore, investigated CCX CKR expression in this inflammatory disease. METHODS AND RESULTS: CCX CKR mRNA was semiquantitated using RT-PCR in unseparated bronchoalveolar (BAL) cells from sarcoidosis patients (S, n = 29) and healthy control subjects (C, n = 9). CCX CKR transcripts were upregulated in patients (mean +/- SEM); S, 0.82 +/- 0.10; C, 0.44 +/- 0.04; p = 0.01; this upregulation paralleled the disease course as assessed by the chest radiographic stage (p < 0.02). Immunocytochemistry localised the CCX CKR protein to ciliated bronchial cells. Flow cytometric fluorescent ligand uptake assay showed that these cells are able to internalize its ligand. CONCLUSION: These observations implicate CCX CKR in the modulation of the inflammatory response in sarcoidosis.
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