Linked Life Data

11994432

Source:http://linkedlifedata.com/resource/pubmed/id/11994432

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pubmed-article:11994432pubmed:abstractTextIL-10 is a potent anti-inflammatory cytokine and inhibitor of TNF-alpha production. The molecular pathways by which IL-10 inhibits TNF-alpha production are obscure, with diverse mechanisms having been published. In this study, a new approach has been taken for the study of human cells. Adenovirus was used to deliver TNF-alpha promoter-based luciferase reporter genes to primary human monocytic cells. The reporter genes were highly responsive to macrophage activation and appeared to mirror the behavior of the endogenous TNF-alpha gene. When added, either with or after the stimulus, IL-10 required the 3' untranslated region of the TNF-alpha gene to inhibit luciferase mRNA and protein expression, indicating a posttranscriptional mechanism. However, if macrophages were incubated with IL-10 before activation, inhibition of gene expression was also mediated by the 5' promoter, suggesting a transcriptional mechanism. To our knowledge, this is the first time that a dual mechanism for IL-10 function has been demonstrated. Studies to elucidate the mechanisms underlying the inhibition of TNF-alpha production addressed the effect of IL-10 on the activation of p38 mitogen-activated protein kinase and NF-kappaB. However, these studies could demonstrate no requirement for the inhibition of p38 mitogen-activated protein kinase or NF-kappaB activation as potential mechanisms. Overall, these results may explain the diversity previously ascribed to the complex mechanisms of IL-10 anti-inflammatory activity.lld:pubmed
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pubmed-article:11994432pubmed:articleTitleEvidence for a dual mechanism for IL-10 suppression of TNF-alpha production that does not involve inhibition of p38 mitogen-activated protein kinase or NF-kappa B in primary human macrophages.lld:pubmed
pubmed-article:11994432pubmed:affiliationKennedy Institute of Rheumatology Division, Imperial College Faculty of Medicine, Charing Cross Campus, 1 Aspenlea Road, London, United Kingdom.lld:pubmed
pubmed-article:11994432pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11994432pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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