作者: Zbigniew Zaslona , Ewelina Flis , Ciara Nulty , Jay Kearney , Rebecca Fitzgerald
DOI: 10.4049/IMMUNOHORIZONS.2000080
关键词: Peritonitis 、 Caspase 4 、 Secretion 、 Immunology 、 Peptic 、 Pyroptosis 、 Inflammasome 、 In vivo 、 Helicobacter pylori 、 Medicine
摘要: Peptic ulcers are caused by the interaction between bacterial and host factors. This study demonstrates enhanced expression of caspase-4 in peptic ulcer patient biopsies, indicating that pyroptosis noncanonical inflammasome activity may be processes involved disease. We show primary murine macrophages infected with Helicobacter pylori upregulate caspase-11 (the ortholog human caspase-4), activate caspase-1, secrete IL-1β. demonstrate misoprostol (a stable PGE1 analogue) decreased IL-1β secretion delayed lethality vivo a peritonitis model. PGE2 was shown to inhibit caspase-11-driven macrophages. Overall, we provide evidence for pathological role caspase-4/11 disease propose targeting or inhibiting have therapeutic potential management ulcers.