Journal
INFECTION AND IMMUNITY
Volume 69, Issue 5, Pages 2847-2852Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.69.5.2847-2852.2001
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Funding
- NIAID NIH HHS [AI/AR 44127, R01 AI044127] Funding Source: Medline
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Lipopolysaccharide (LPS) is a very potent inducer of tumor necrosis factor alpha (TNF-alpha) expression from monocytes and macrophages, Another inflammatory cytokine, gamma interferon (IFN-gamma), can potentiate the effects of LPS, but the mechanism is not thoroughly understood. Previous reports emphasized the ability of IFN-gamma to upregulate CD14 expression (the receptor for LPS), and nearly all studies hare utilized sequential stimulation with IFN-gamma followed by LPS to exploit this phenomenon. This study demonstrates that IFN-gamma can upregulate the effect of LPS at the level of transcription. Human monoblastic Mono-Mac-6 cells produced up to threefold-greater levels of TNF-alpha when simultaneously stimulated with LPS and IFN-gamma compared to treatment with LPS alone. RNase protection studies showed a similar increase in RNA beginning as early as within 30 min. The synthesis of TNF-alpha mRNA in IFN-gamma- and LPS treated Mono-Mac-6 cells was also temporally prolonged even though the message turnover rate was identical to that seen in LPS stimulated cells. The modulatory effect of IFN-gamma mag be mediated by Jak2.
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