Antagonism by IL-4 and IL-10 of Endotoxin-Induced Tissue Factor Activation in Monocytic THP-1 Cells: Activating Role of CD14 Ligation

Chu, Arthur J.; Prasad, J.K.

doi:10.1006/jsre.1998.5346

Cited by 23 publications

(18 citation statements)

References 41 publications

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“…Concerning LPS mimicking action, CD14 ligation with anti-CD14 mAb was able to produce as much as ϳ35% of the TF activation and NO elicitation induced by LPS. Therefore, the data suggest that CD14 governs at least 70 -75% of LPS transmembrane signaling [10], which is in good agreement with the current finding that 75% FITC-LPS binding is blocked by anti-CD14 mAb (Fig. 2).…”

supporting

confidence: 92%

“…In transgenic mice, the overexpression of hCD14 has been reported to become more sensitive to LPS compared with that of normals [41]. Transfection of 70Z/3 cells with hCD14 maximized LPS sensitivity [42], which lent further support to the essential role of CD14 in LPS response.Our recent study [10] has extended the importance of CD14 with twofold significance in triggering LPS action. CD14 not only transmitted LPS signal, but also mimicked LPS action on ligation.…”

mentioning

confidence: 95%

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Blockade by Polyunsaturated n-3 Fatty Acids of Endotoxin-Induced Monocytic Tissue Factor Activation Is Mediated by the Depressed Receptor Expression in THP-1 Cells

Chu¹,

Walton

Prasad

et al. 1999

Journal of Surgical Research

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confidence: 92%

mentioning

confidence: 95%

Blockade by Polyunsaturated n-3 Fatty Acids of Endotoxin-Induced Monocytic Tissue Factor Activation Is Mediated by the Depressed Receptor Expression in THP-1 Cells

Chu¹,

Walton

Prasad

et al. 1999

Journal of Surgical Research

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“…Several studies indicate that the interaction between LPS or gram-positive bacterial components and the CD14 molecule expressed on monocytes is a prerequisite to initiation of the early cascade of signaling events involved in cytokine synthesis (7,20,22,28,31,34,43). However, previous data suggest that other CD14-independent mechanisms may trigger cell activation (26,33,42,51).…”

Section: Resultsmentioning

confidence: 99%

Gram-Positive and Gram-Negative Bacteria Do Not Trigger Monocytic Cytokine Production through Similar Intracellular Pathways

et al. 2001

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Toll-like receptors (TLRs) are involved in human monocyte activation by lipopolysaccharide (LPS) andStaphylococcus aureus Cowan (SAC), suggesting that gram-positive and gram-negative bacteria may trigger similar intracellular events. Treatment with specific kinase inhibitors prior to cell stimulation dramatically decreased LPS-induced cytokine production. Blocking of the p38 pathway prior to LPS stimulation decreased interleukin-1␣ (IL-1␣), IL-1ra, and tumor necrosis factor alpha (TNF-␣) production, whereas blocking of the ERK1/2 pathways inhibited IL-1␣, IL-1␤, and IL-1ra but not TNF-␣ production. When cells were stimulated by SAC, inhibition of the p38 pathway did not affect cytokine production, whereas only IL-1␣ production was decreased in the presence of ERK kinase inhibitor. We also demonstrated that although LPS and SAC have been shown to bind to CD14 before transmitting signals to TLR4 and TLR2, respectively, internalization of CD14 occurred only in monocytes triggered by LPS. Pretreatment of the cells with SB203580, U0126, or a mixture of both inhibitors did not affect internalization of CD14. Altogether, these results suggest that TLR2 signaling does not involve p38 mitogen-activated protein kinase signaling pathways, indicating that divergent pathways are triggered by gram-positive and gram-negative bacteria, thereby inducing cytokine production.Invasive infection by gram-positive and gram-negative bacteria in humans results in septic shock and death. The early cellular response to both groups of microorganisms is still unclear. Several investigators have proposed that lipopolysaccharides (LPS) from gram-negative bacteria, as well as several components from gram-positive bacteria, trigger monocytic cytokine production following interaction with membrane-bound CD14 (mCD14) and activation of Toll-like receptors (TLRs; the human homologues of Drosophila Toll) which are present on the cell membrane (23,30,43,61). Several lines of evidence suggest that after binding to mC14, LPS initiates intracellular signaling pathways activating a number of tyrosine kinases as an initial step. Various ␣ subunits of heterodimeric G proteins and Src kinases, physically associated with membrane-bound CD14 molecules in LPS-stimulated normal human monocytes, induce p38 mitogen-activated protein (MAP) kinase activation, which is involved in cytokine synthesis (44). Other proteins that are phosphorylated upon LPS stimulation include p42 and p44 MAP kinases, which are encoded by the erk2 and erk1 genes, respectively (10, 25). However, the upstream events that occur during ERK1, ERK2, and p38 kinase phosphorylation remain unclear. There is some evidence that LPS activates Ras and consequently Raf, resulting in MEK-1 and MAP kinase phosphorylation, but the precise pathways are not fully understood (8). In addition to MEK and MAP kinase activation, Syk molecules are phosphorylated upon LPS stimulation of macrophages. However, several studies have indicated that neither Syk, Src family tyrosine kinases, Hck, Lyn, nor Fgr is indispe...

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“…This is consistent with several previous studies that demonstrated an IL-10 mediated reduction of TF activity, protein, and mRNA expression. 25,32,33 We extended those studies to evaluate the molecular pathways underlying the inhibitory effects of IL-10 on TF expression. The classical pathway of TF induction by LPS involves binding of LPS to the Toll-like receptor 4 (TLR4), followed by the activation of several intracellular pathways.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-10 Suppresses Tissue Factor Expression in Lipopolysaccharide-Stimulated Macrophages via Inhibition of Egr-1 and a Serum Response Element/MEK-ERK1/2 Pathway

Kamimura

Viedt

Dalpke

et al. 2005

Circulation Research

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Abstract-Atherosclerosis is considered to be an inflammatory disease. Tissue factor (TF), a prothrombotic molecule expressed by various cell types within atherosclerotic plaques, is thought to play an essential role in thrombus formation after atherosclerotic plaque rupture. Recent studies suggest that the antiinflammatory cytokine interleukin-10 (IL-10) has many antiatherosclerotic properties. Therefore, the effects of IL-10 on TF expression in response to inflammation were investigated. Mouse macrophages were stimulated with lipopolysaccharide (LPS) in the presence or absence of IL-10. Pretreatment with IL-10 resulted in a 50% decrease in TF mRNA expression and TF promoter activity. Binding of early growth response gene-1 (Egr-1) to the consensus DNA sequence, a key transcriptional activator of TF expression in response to inflammation, and the expression of Egr-1 mRNA were also inhibited by IL-10. This inhibition was independent of the induction of suppressor of cytokine signaling protein-3 by IL-10. Macrophages that had been transfected with luciferase reporter constructs containing the murine Egr-1 5Ј-flanking sequence exhibited reduced reporter gene activity in response to LPS stimulation with IL-10 pretreatment. Studies with deletion constructs of the Egr-1 promoter identified the proximal serum response element SRE3 as a potential regulatory site for the IL-10 mediated suppression of Egr-1 expression. Furthermore, activation of the upstream signal-transduction elements, such as mitogen-activated protein kinase kinase (MEK) 1/2, extracellular signal-regulated kinase 1/2, and Elk-1 were also inhibited by IL-10 pretreatment. Taken

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Antagonism by IL-4 and IL-10 of Endotoxin-Induced Tissue Factor Activation in Monocytic THP-1 Cells: Activating Role of CD14 Ligation

Cited by 23 publications

References 41 publications

Blockade by Polyunsaturated n-3 Fatty Acids of Endotoxin-Induced Monocytic Tissue Factor Activation Is Mediated by the Depressed Receptor Expression in THP-1 Cells

Blockade by Polyunsaturated n-3 Fatty Acids of Endotoxin-Induced Monocytic Tissue Factor Activation Is Mediated by the Depressed Receptor Expression in THP-1 Cells

Gram-Positive and Gram-Negative Bacteria Do Not Trigger Monocytic Cytokine Production through Similar Intracellular Pathways

Interleukin-10 Suppresses Tissue Factor Expression in Lipopolysaccharide-Stimulated Macrophages via Inhibition of Egr-1 and a Serum Response Element/MEK-ERK1/2 Pathway

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