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• W2149255038 abstract "Background Eotaxin is implicated in asthmatic eosinophilia. Oncostatin M (OSM) causes eotaxin release from fibroblasts. Objective We sought to examine the effects and mechanism of action of OSM and other IL-6 family cytokines on eotaxin release from human airway smooth muscle cells. Methods Eotaxin 1 release was measured by means of ELISA. Western blotting was used to examine mitogen-activated protein kinase and signal transducer and activator of transcription 3 (STAT-3) phosphorylation. Eotaxin promoter activity was analyzed in cells transfected with wild-type STAT-3, a mutant form of STAT-3 that cannot be phosphorylated, and a constitutively active form of STAT-3. The mRNA and protein expression of IL-4Rα, the signaling receptor for IL-4 and IL-13, was evaluated by means of real-time PCR and flow cytometry, respectively. Results OSM increased eotaxin 1 release and augmented IL-4– or IL-13–induced eotaxin release, whereas other IL-6 family cytokines did not. OSM caused a greater increase in STAT-3 phosphorylation and STAT-3–mediated gene transcription than other IL-6 family cytokines. OSM increased eotaxin promoter activity and augmented IL-13– and IL-4–induced increases in promoter activity. The constitutively active form of STAT-3 increased eotaxin promoter activity, whereas the mutant form of STAT-3 that cannot be phosphorylated significantly reduced eotaxin promoter activity induced by OSM or IL-4 plus OSM. OSM increased IL-4Rα mRNA and protein levels. Conclusions OSM induces eotaxin 1 expression in human airway smooth muscle cells by a mechanism involving STAT-3. OSM synergizes with IL-13 and IL-4 to increase eotaxin 1 expression, possibly as a result of effects on IL-4Rα expression." @default.
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• W2149255038 date "2005-03-01" @default.
• W2149255038 modified "2023-09-27" @default.
• W2149255038 title "Oncostatin M causes eotaxin-1 release from airway smooth muscle: Synergy with IL-4 and IL-13" @default.
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• W2149255038 doi "https://doi.org/10.1016/j.jaci.2004.11.033" @default.
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