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• W2029063753 abstract "RATIONALE: Asthma is a complex polygenic disorder characterized by airway inflammation. IL-4 and IL-13 are critical Th2 cytokines in the allergic cascade and in the pathogenesis of asthma. One mechanism by which IL-4 and IL-13 perpetuate the allergic inflammatory cascade is by increasing cysteinyl leukotriene receptor 1 (CysLT1R) expression and consequently increasing responsiveness to cysteinyl leukotrienes (CysLTs). Since IL-4 and IL-13 affect the CysLT pathway, it is likely that the CysLTs also affect the IL-4 and IL-13 pathways. We examined the direct effects of CysLTs on IL-4 and IL-13 signaling pathways and the direct impact of IL-4 on CysLT signaling.METHODS: The human monocyte cell line U937 responds to IL-4 and IL-13 by activating Stat6. These cells also respond to CysLTs by calcium mobilization. We pretreated U937 cells with various concentrations of CysLTs for varying periods of time and assessed maximal and half-max IL-4 and IL-13 dependent Stat6 activation by electrophoretic mobility shift assay. We also examined the direct effect of IL-4 on CysLT signaling by pretreating U937 cells with IL-4 and determining CysLT dependent calcium flux.RESULTS: Pretreatment of U937 cells with CysLTs did not alter maximal or half-max IL-4 or IL-13 dependent Stat6 activation. Pretreatment of U937 cells with IL-4 for up to 24 hours did not affect CysLT dependent calcium mobilization.CONCLUSIONS: While IL-4 is reported to increases CysLT1R expression, short treatment with IL-4 does not affect CysLTs signaling by calcium mobilization. CysLTs have no direct effect on IL-4 or IL-13 dependent Stat6 activation. RATIONALE: Asthma is a complex polygenic disorder characterized by airway inflammation. IL-4 and IL-13 are critical Th2 cytokines in the allergic cascade and in the pathogenesis of asthma. One mechanism by which IL-4 and IL-13 perpetuate the allergic inflammatory cascade is by increasing cysteinyl leukotriene receptor 1 (CysLT1R) expression and consequently increasing responsiveness to cysteinyl leukotrienes (CysLTs). Since IL-4 and IL-13 affect the CysLT pathway, it is likely that the CysLTs also affect the IL-4 and IL-13 pathways. We examined the direct effects of CysLTs on IL-4 and IL-13 signaling pathways and the direct impact of IL-4 on CysLT signaling. METHODS: The human monocyte cell line U937 responds to IL-4 and IL-13 by activating Stat6. These cells also respond to CysLTs by calcium mobilization. We pretreated U937 cells with various concentrations of CysLTs for varying periods of time and assessed maximal and half-max IL-4 and IL-13 dependent Stat6 activation by electrophoretic mobility shift assay. We also examined the direct effect of IL-4 on CysLT signaling by pretreating U937 cells with IL-4 and determining CysLT dependent calcium flux. RESULTS: Pretreatment of U937 cells with CysLTs did not alter maximal or half-max IL-4 or IL-13 dependent Stat6 activation. Pretreatment of U937 cells with IL-4 for up to 24 hours did not affect CysLT dependent calcium mobilization. CONCLUSIONS: While IL-4 is reported to increases CysLT1R expression, short treatment with IL-4 does not affect CysLTs signaling by calcium mobilization. CysLTs have no direct effect on IL-4 or IL-13 dependent Stat6 activation." @default.
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• W2029063753 date "2007-01-01" @default.
• W2029063753 modified "2023-09-27" @default.
• W2029063753 title "Signaling Interactions Between IL-4 or IL-13 and Leukotrienes in Allergic Inflammation" @default.
• W2029063753 doi "https://doi.org/10.1016/j.jaci.2006.12.500" @default.
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