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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
1997-8-1
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pubmed:abstractText |
Pharmacological control of interleukin-12 (IL-12) production may be a key therapeutic strategy for modulating immunological diseases dominated by type-1 cytokine responses. In this study, we investigated the effects of pentoxifylline on the production of IL-12 by human blood mononuclear cells and primary human monocytes stimulated with heat-killed Staphylococcus aureus Cowan strain I (SAC) or lipopolysaccharide (LPS). Pentoxifylline potently suppressed production of IL-12 in a concentration-dependent manner. In these same experiments, tumour necrosis factor-alpha (TNF-alpha) production was inhibited and IL-10 and prostaglandin E2 (PGE2) production was enhanced by treatment with pentoxifylline. Suppression of IL-12 production by pentoxifylline was found to be independent of several known endogenous inhibitors of IL-12, such as IL-10, transforming growth factor-beta (TGF-beta), IL-4 and PGE2. RNase protection assays revealed that pentoxifylline inhibited accumulation of both IL-12 p40 and p35 mRNA, suggesting a predominant mRNA locus for pentoxifylline-induced IL-12 inhibition. Low levels of pentoxifylline added to the suppression of IL-12 production by suboptimal inhibiting doses of dexamethasone, suggesting that this drug combination may have therapeutic utility. These results provide a firm rationale for the use of pentoxifylline in clinical trials of immunological disorders characterized by inappropriate type-1 immune responses.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9227317-1357073,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9227317-1358972,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9227317-1360994,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9227317-2574766,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9227317-8816374
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0019-2805
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
91
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
197-203
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9227317-Cell Culture Techniques,
pubmed-meshheading:9227317-Dexamethasone,
pubmed-meshheading:9227317-Dose-Response Relationship, Drug,
pubmed-meshheading:9227317-Humans,
pubmed-meshheading:9227317-Indomethacin,
pubmed-meshheading:9227317-Interleukin-10,
pubmed-meshheading:9227317-Interleukin-12,
pubmed-meshheading:9227317-Leukocytes, Mononuclear,
pubmed-meshheading:9227317-Monocytes,
pubmed-meshheading:9227317-Pentoxifylline,
pubmed-meshheading:9227317-RNA, Messenger,
pubmed-meshheading:9227317-Transforming Growth Factor beta
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pubmed:year |
1997
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pubmed:articleTitle |
Inhibition of human interleukin-12 production by pentoxifylline.
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pubmed:affiliation |
Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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