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- W2321536052 abstract "Interleukin-1beta (IL-1β) is the most bioactive proinflammatory cytokine in acute lung injury (ALI). Secretion of IL-1β causes activation of alveolar epithelial cells which propagates this inflammatory response. Recently a lipid mediator, termed aspirin triggered resolvin D1 (AT-RvD1), attenuated inflammation in response to acute injury, however, the effects of AT-RVD1 on IL-1β induced epithelial cell activation has not been investigated. We hypothesize that AT-RvD1 decreases IL-1β induced alveolar epithelial cell activation. Human alveolar epithelial cells were treated with IL-1β (10ng) in the presence or absence of AT-RVD1 (.01-.1μM) at varying time points. After each time point, Cells were harvested to assess the expression levels of protein and RNA by western blot and qPCR analysis respectively. Cell culture supernatants were collected to analyze cytokine secretion via ELISA. In a separate experiment, alveolar epithelial cells were fixed for immunocytochemical analysis. Results indicate that AT-RvD1 significantly inhibited IL-1β induced TGF-β and IL-6 secretion in alveolar epithelial cells. AT-RvD1 also inhibits IL-1β mediated p38 MAPK phosphorylation. Finally, IL-1β induced alveolar epithelial cell permeability was decreased in AT-RvD1 treated cells. Alveolar macrophages and epithelial cells are sentinel cells that sense and respond to injury as a result of cytokine signaling. During ALI, excessive secretion of IL-1β leads to an unregulated immune response hallmarked by activated macrophages, epithelial and endothelial cells. Therefore, AT-RvD1, by inhibiting epithelial cell activation, could be a useful therapeutic for ALI." @default.
- W2321536052 created "2016-06-24" @default.
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- W2321536052 date "2013-02-01" @default.
- W2321536052 modified "2023-09-26" @default.
- W2321536052 title "Resolvin D1 Inhibits IL-1beta Induced Alveolar Epithelial Cell Activation" @default.
- W2321536052 doi "https://doi.org/10.1016/j.jaci.2012.12.1370" @default.
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