Linked Life Data

10489835

Source:http://linkedlifedata.com/resource/pubmed/id/10489835

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-10-21
pubmed:abstractText
Reactive oxygen intermediates exert signalling functions and modulate gene transcription, particularly for pro-inflammatory cytokines. Since exogenous as well as endogenous thiols could be potent inhibitors of the production of cytokines, the effects of N-acetylcysteine (NAC), glutathione (GSH) and modulated GSH synthesis on the production of tumour necrosis factor (TNF)-alpha, interleukin (IL)-6 and IL-8 by human alveolar macrophages (AMs) was evaluated, as well as the potential role of intracellular GSH depletion on the effect of exogenous thiols. AMs were stimulated with lipopolysaccharide (LPS) and cytokine production was measured by evaluating messenger ribonucleic acid (mRNA) expression and protein secretion. Depletion of intracellular GSH by treatment with buthionine sulphoximine (BSO) reached 45.2% after 3 h and was nearly complete at 24 h. Whereas a 24-h preincubation of AMs with BSO significantly increased LPS-induced secretion of TNF-alpha and IL-8, a 3-h preincubation only enhanced LPS-stimulated production of IL-8 (p<0.05). Treatment with NAC and GSH did not significantly increase intracellular content of GSH even after a 48-h incubation. Addition of GSH and NAC significantly reduced the secretion of TNF-alpha (mean+/-SEM 21.2+/-5 and 44.7+/-4.4% inhibition, respectively) as well as LPS-induced IL-6 and IL-8 (p<0.05). Similarly, NAC inhibited the production of TNF-alpha, IL-6 and IL-8 in GSH-depleted AMs obtained by BSO pretreatment. In conclusion, N-acetylcysteine and glutathione inhibit the production of tumour necrosis factor-alpha, interleukin-8 and interleukin-6 by alveolar macrophages by a mechanism independent of glutathione metabolism. However, total depletion of glutathione within alveolar macrophages significantly increases tumour necrosis factor-alpha and interleukin-8 synthesis whereas it does not modulate interleukin-6 secretion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0903-1936
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
98-105
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10489835-Acetylcysteine, pubmed-meshheading:10489835-Adult, pubmed-meshheading:10489835-Antimetabolites, pubmed-meshheading:10489835-Antioxidants, pubmed-meshheading:10489835-Buthionine Sulfoximine, pubmed-meshheading:10489835-Cells, Cultured, pubmed-meshheading:10489835-DNA Primers, pubmed-meshheading:10489835-Female, pubmed-meshheading:10489835-Glutathione, pubmed-meshheading:10489835-Humans, pubmed-meshheading:10489835-Interleukin-6, pubmed-meshheading:10489835-Interleukin-8, pubmed-meshheading:10489835-Intracellular Fluid, pubmed-meshheading:10489835-Lipopolysaccharides, pubmed-meshheading:10489835-Macrophages, Alveolar, pubmed-meshheading:10489835-Male, pubmed-meshheading:10489835-Polymerase Chain Reaction, pubmed-meshheading:10489835-RNA, Messenger, pubmed-meshheading:10489835-Tumor Necrosis Factor-alpha
pubmed:year
1999
pubmed:articleTitle
Thiol regulation of the production of TNF-alpha, IL-6 and IL-8 by human alveolar macrophages.
pubmed:affiliation
Unité INSERM U416, Institut Pasteur, Lille, France.
pubmed:publicationType
Journal Article, Comparative Study