Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-9-23
pubmed:abstractText
Corticosteroids are the most effective drugs in the management of asthma. However, because of their known side effects and the existence of corticosteroid-resistant patients, there is a need for substitute medications in asthma therapy. Using cell lines, in the present study, the two corticosteroids dexamethasone (Dex), and beclomethasone (Bec), as well as the immunosuppressant cyclosporin A (CsA), and the antimetabolic drug methotrexate (Mtx) were examined in their effect on release of immunoreactive IL-1 beta, IL-2, IL-4, IL-5, and IL-8. THP-1 cells served as a test model for monocytes secreting IL-1 beta and IL-8 upon stimulation by lipopolysaccharide. Jurkat cells were used as a test model for TH1-type T-cells and were stimulated for IL-2 release with a combination of phytohemagglutinin and phorbol myristate acetate. Representing TH2-type T-cells, D10.G4.1 cells challenged by anti-CD3-mAb produced IL-4, and IL-5. Considerable qualitative and quantitative differences in the relative efficacy of the test compounds were found. Following IC50 values (nmol/l) of the test compounds were estimated (IL-1 beta/IL-8/IL-2/IL-4/IL-5): Dex (10.8/35.7/ > 10,000.0/5.1/4.1), Bec (30.9/102.2/8591.4/0.6/0.4), and CsA (318.7/6211.2/2.3/68.2/237.9). Mtx in concentrations up to 10,000.0 nmol/l was completely inactive. It can be concluded that corticosteroids show another inhibition pattern than CsA: corticosteroids affect mainly TH2-type T-cells, while CsA primarily inhibits the TH1-type T-cell response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0162-3109
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
173-9
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:articleTitle
Effect of corticosteroids, cyclosporin A, and methotrexate on cytokine release from monocytes and T-cell subsets.
pubmed:affiliation
Department of Pharmacology, ASTA Medica AG, Frankfurt/Main, Germany.
pubmed:publicationType
Journal Article