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Limited By:	Subject = Pyroptosis;

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Caspase-11 promotes allergic airway inflammation (2020)

Creagh, Emma; Lavelle, Edward; O'Neill, Luke; Mills, Kingston; Zas?ona, Zbigniew; ...

Caspase-11 promotes allergic airway inflammation (2020)

Creagh, Emma; Lavelle, Edward; O'Neill, Luke; Mills, Kingston; Zas?ona, Zbigniew; Flis, Ewelina; Wilk, Mieszko M.; Carroll, Richard G.; Palsson-McDermott, Eva M.; Hughes, Mark M.; Diskin, Ciana; Banahan, Kathy; Ryan, Dylan G.; Hooftman, Alexander; Misiak, Alicja; Kearney, Jay; Lochnit, Gunter; Bertrams, Wilhelm; Greulich, Timm; Schmeck, Bernd

Abstract:

Activated caspase-1 and caspase-11 induce inflammatory cell death in a process termed pyroptosis. Here we show that Prostaglandin E2 (PGE2) inhibits caspase-11-dependent pyroptosis in murine and human macrophages. PGE2 suppreses caspase-11 expression in murine and human macrophages and in the airways of mice with allergic inflammation. Remarkably, caspase-11-deficient mice are strongly resistant to developing experimental allergic airway inflammation, where PGE2 is known to be protective. Expression of caspase-11 is elevated in the lung of wild type mice with allergic airway inflammation. Blocking PGE2 production with indomethacin enhances, whereas the prostaglandin E1 analog misoprostol inhibits lung caspase-11 expression. Finally, alveolar macrophages from asthma patients exhibit increased expression of caspase-4, a human homologue of caspase-11. Our findings identify PGE2 as a negative regulator of caspase-11-driven pyroptosis and implicate caspase-4/11 as a critical contributor ...