In vitro pharmacoregulation of CC chemokine ligand 5 and its receptor CCR5 in diffuse lung diseases
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
14514472
PubMed Central
PMC1781614
DOI
10.1080/09629350310001599657
PII: ND1QJKHLL7GV6WRP
Knihovny.cz E-zdroje
- MeSH
- bronchoalveolární lavážní tekutina cytologie MeSH
- chemokin CCL5 MeSH
- chemokiny CC genetika metabolismus MeSH
- cyklosporin farmakologie MeSH
- dexamethason farmakologie MeSH
- dospělí MeSH
- glukokortikoidy farmakologie MeSH
- imunosupresiva farmakologie MeSH
- inhibitory enzymů farmakologie MeSH
- kultivované buňky MeSH
- leukocyty cytologie účinky léků imunologie metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- messenger RNA metabolismus MeSH
- pentoxifylin farmakologie MeSH
- plicní nemoci metabolismus patologie MeSH
- receptory CCR5 genetika metabolismus MeSH
- senioři MeSH
- TNF-alfa farmakologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- CCL5 protein, human MeSH Prohlížeč
- chemokin CCL5 MeSH
- chemokiny CC MeSH
- cyklosporin MeSH
- dexamethason MeSH
- glukokortikoidy MeSH
- imunosupresiva MeSH
- inhibitory enzymů MeSH
- messenger RNA MeSH
- pentoxifylin MeSH
- receptory CCR5 MeSH
- TNF-alfa MeSH
BACKGROUND: CC chemokine ligand (CCL)5 and its receptor CCR5 contribute to leukocyte migration into lungs of patients with diffuse lung diseases (DLD). Pharmacological regulation of CCL5 and CCR5 expression was therefore explored in bronchoalveolar cells obtained from patients with DLD. METHODS: Cells from 21 patients were co-cultivated in vitro with tumour necrosis factor-alpha and dexamethasone, cyclosporin A (CyA) or pentoxifylline. Chemokine mRNA expression and protein production was assessed by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. RESULTS: Dexamethasone altered CCL5 mRNA expression and suppressed its protein levels. CyA inhibited chemokine mRNA expression but not protein production. Pentoxifylline did not affected chemokine expression. Both dexamethasone and CyA suppressed CCR5 mRNA transcripts. CONCLUSION: In conclusion, while dexamethasone downregulates the CCL5 functional form, CyA and pentoxifylline have no effects on CCL5 protein. These data provide in vitro correlation for clinical applications of immunomodulators in therapy of DLD.
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