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  • 1
    Electronic Resource
    Electronic Resource
    Role of mitogen-activated protein kinases in influenza virus induction of prostaglandin E2 from arachidonic acid in bronchial epithelial cells (2003)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 33 (2003), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Influenza virus (IV) infection causes airway inflammation; however, it has not been determined whether IV infection could catabolize arachidonic acid cascade in airway epithelial cells. In addition, the responsible intracellular signalling molecules that catabolize arachidonic acid cascade have not been determined.Objective In the present study, to clarify these issues, we examined the cyclooxygenase (COX) expression, cytosolic phospholipase A2 (cPLA2) phosphorylation and prostaglandin E2 (PGE2) release in human bronchial epithelial cells (BEC) upon IV infection, and the role of mitogen-activated protein kinase (MAPK) including extracellular signal-regulated kinase (ERK), p38 MAPK and c-Jun-NH2-terminal kinase (JNK) in catabolizing arachidonic acid cascade in BEC.Methods COX-2 expression, phosphorylation of cPLA2 and phosphorylation of ERK, JNK and p38 MAPK were determined by Western blot. The concentrations of PGE2 were determined by ELISA. PD 98059 as a specific inhibitor of MAPK kinase-1 (MEK-1), an up-stream kinase of ERK, SB 203580 as a specific inhibitor of p38 MAPK and CEP-11004 as a specific inhibitor of JNK cascade were used to investigate the role of ERK, p38 MAPK and JNK in catabolizing arachidonic acid cascade in BEC.Results The results showed that (1) IV infection increases COX-2 expression, cPLA2 phosphorylation and PGE2 release, (2) ERK, p38 MAPK and JNK were phosphorylated, (3) CEP-11004 and PD 98059 predominantly attenuated COX-2 expression and cPLA2 phosphorylation, respectively, (4) SB 203580 did not remarkably affect COX-2 expression and cPLA2 phosphorylation, and (5) each inhibitor dose-dependently attenuated PGE2 release by various extents.Conclusion These results indicate that IV infection activates three distinct MAPKs, ERK, p38 MAPK and JNK, to participate to various extents in the induction of PGE2 synthesis from arachidonic acid in BEC.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.2003.01750.x
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  • 2
    Electronic Resource
    Electronic Resource
    Intracellular glutathione regulates tumour necrosis factor-α-induced p38 MAP kinase activation and RANTES production by human bronchial epithelial cells (2001)
    Oxford, UK : Blackwell Science, Ltd
    Clinical & experimental allergy 31 (2001), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: RANTES plays an important role in the production of allergic inflammation of the airway through its chemotactic activity for eosinophils. The cellular reduction and oxidation (redox) changes are involved in the activation of p38 mitogen-activated protein (MAP) kinase and the induction of cytokine expression. It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFα is inversely correlated with cellular redox state. However, a role of cellular redox regulated by intracellular glutathione (GSH) in TNFα-induced p38 MAP kinase activation and p38 MAP kinase-mediated RANTES production by human BECs has not been determined.Human BECs were exposed to NAC or buthionine sulfoximine (BSO). TNFα-induced p38 MAP kinase activation and p38 MAP kinase-mediated RANTES production by human BECs were then examined in order to clarify these issues.The results showed that: NAC attenuated TNFα-induced p38 MAP kinase activation and RANTES production; SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-α-induced RANTES production; BSO facilitated TNF-α-induced p38 MAP kinase activation and RANTES production; SB 203580 attenuated BSO-mediated facilitation of TNF-α-induced RANTES production; and the intracellular GSH increased in NAC-treated cells, whereas the intracellular GSH was reduced in BSO-treated cells.These results indicate that cellular redox regulated by GSH is critical for TNF-α-induced p38 MAP kinase activation and p38 MAP kinase-mediated RANTES production by human BECs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2001.00967.x
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  • 3
    Electronic Resource
    Electronic Resource
    Common and distinct signalling cascades in the production of tumour necrosis factor-α and interleukin-13 induced by lipopolysaccharide in RBL-2H3 cells (2005)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 35 (2005), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Activation of mast cells by lipopolysaccharide (LPS) results in the production of TNF-α and IL-13. TNF-α and IL-13 are key mediators in the development of neutrophilic and allergic inflammation, respectively. LPS-induced TNF-α and IL-13 production in mast cells has been reported to be mediated by Toll-like receptor 4 (TLR4) signalling, but differences in signal transduction mechanisms leading to the production of these cytokines are not clearly defined.Objective We investigated the molecular mechanisms responsible for LPS-induced TNF-α and IL-13 production in mast cells.Methods TNF-α and IL-13 production by LPS was assessed by transfecting RBL-2H3 cells with dominant-negative (DN) expression vectors.Results Transfection of RBL-2H3 cells with plasmids encoding DN mutants of myeloid differentiation protein (MyD88) and TNFR-associated factor (TRAF6) inhibited both LPS-induced TNF-α and IL-13 production. IκBα-DN inhibited LPS-induced production of TNF-α, but not IL-13. We also found that inhibition of p38 kinase suppressed both TNF-α and IL-13 induction by LPS, and inhibition of JNK reduced IL-13 production, but not TNF-α. Furthermore, we found that protein kinase R (PKR) was activated by LPS in these cells. Treatment with 2-aminopurine, a PKR inhibitor, attenuated LPS-induced nuclear factor-κB activation and TNF-α production, whereas inhibition of PKR had little effect on IL-13 production.Conclusion These findings indicate that the production of TNF-α and IL-13 by LPS required TLR4/MyD88/TRAF6 signalling as a common pathway of mast cell-mediated inflammation. We furthermore found that TNF-α and IL-13 production were differentially regulated by signalling cascades through PKR and mitogen-activated protein kinases downstream of TRAF6 in mast cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2005.02223.x
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  • 4
    Electronic Resource
    Electronic Resource
    TNF-α Regulates GM-CSF-, IL-3- or M-CSF-Induced Fc ε RII/CD23 Gene Expression and Soluble Fc ε RII Release by Human Monocytes (1997)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 45 (1997), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The authors examined the regulatory effects of tumour necrosis factor-α (TNF-α) on granulocyte macrophage colony stimulating factor (GM-CSF)-, interleukin-3 (IL-3)- or macrophage colony stimulating factor (M-CSF)-induced gene expression of the low affinity receptor for IgE (Fc ε RII) on human monocytes and GM-CSF-, IL-3- or M-CSF-induced soluble Fc ε RII (sFc ε RII) release from monocytes. The expression of GM-CSF-, IL-3- or M-CSF-induced Fc ε RII on the surface of monocytes was reduced by TNF-α. The present analysis was designed to examine whether or not TNF-α could suppress GM-CSF-, IL-3- or M-CSF-induced Fc ε RII messenger RNA (mRNA) expression and enhance the release of sFc ε RII induced by these cytokines. The addition of TNF-α to monocyte cultures with GM-CSF, IL-3 or M-CSF significantly reduced Fc ε RII expression on the surface of monocytes and significantly increased sFc ε RII release from monocytes. These results suggest that TNF-α-dependent reduction of GM-CSF-, IL-3- or M-CSF-induced Fc ε RII expression on the surface of monocytes resulted, at least in part, from the suppression of Fc ε RII mRNA and the enhancement of sFc ε RII release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1997.d01-396.x
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  • 5
    Electronic Resource
    Electronic Resource
    Regulation by intracellular glutathione of TNF-α-induced p38 MAP kinase activation and RANTES production by human pulmonary vascular endothelial cells (2000)
    Copenhagen : Munksgaard International Publishers
    Allergy 55 (2000), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Conclusions: These results indicated that TNF-α-induced p38 MAP kinase activation and p38 MAP kinase-mediated RANTES production by human pulmonary vascular endothelial cells are inversely regulated by intracellular GSH levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.2000.00455.x
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  • 6
    Electronic Resource
    Electronic Resource
    N-acetylcysteine attenuates TNF-α-dependent reduction of IL-4-induced Fcɛ RII expression in human monocytes (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 52 (1997), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have previously shown that tumor necrosis factor-a (TNF-α) reduces interleukin-4 (IL-4)-induced Fce RII expression in human monocytes. It has been shown that TNF-α activates nuclear transcriptional factors through the generation of reactive oxygen intermediates (ROIs), and antioxidant N-acetylcysteine (NAC) inhibits TNF-α-induced activation of nuclear transcriptional factors. Therefore, we hypothesized that TNF-α-dependent reduction of IL-4-induced Fce RII expression in monocytes might be mediated through the ROIs-activated mechanism. In the present study, to test our hypothesis, we examined the effect of NAC on TNF-α-dependent reduction of IL-4-induced FcɛRII expression in human monocytes. NAC attenuated TNF-α-dependent reduction of IL-4-induced Fcɛ RII expression by attenuating TNF-a-dependent reduction of Fcɛ RII mRNA expression. Similarly, the structurally unrelated antioxidant, pyrrolidine dithiocarbamate (PDTC), also effectively attenuated this reduction. These results indicate that an ROIs-activated and antioxidant-sensitive mechanism might be involved in TNF-α-dependent reduction of IL-4-induced FcɛRII expression in monocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1997.tb01250.x
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  • 7
    Electronic Resource
    Electronic Resource
    p38 MAP kinase regulates RANTES production byTNF-α-stimulated human pulmonary vascular endothelial cells (1999)
    Copenhagen : Munksgaard International Publishers
    Allergy 54 (1999), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: RANTES plays an important role in the production of allergic inflammation of the airway through its chemotactic activity for eosinophils. However, the intracellular signal regulating RANTES expression in human pulmonary vascular endothelial cells has not been determined. In the present study, therefore, we examined the role of p38 mitogen-activated protein (MAP) kinase in RANTES production by tumor necrosis factor (TNF)-α-stimulated pulmonary vascular endothelial cells in order to clarify the signal transduction pathway regulating RANTES production by pulmonary vascular endothelial cells. Methods: We examined p38 MAP kinase activation, and the effect of SB 203580, as the specific inhibitor for p38 MAP kinase, on p38 MAP kinase activity and RANTES production by TNF-α-stimulated human pulmonary vascular endothelial cells. Results: The results showed that TNF-α induced RANTES production and p38 MAP kinase activity in human pulmonary vascular endothelial cells. Abrogation of p38 MAP kinase activity by SB 203580 repressed TNF-α-induced p38 MAP kinase activity and RANTES production. Conclusions: These results indicate that p38 MAP kinase plays an important role in the TNF-α-activated signaling pathway which regulates RANTES production by human pulmonary vascular endothelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.1999.00224.x
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