Inducible CYP2J2 and Its Product 11,12-EET Promotes Bacterial Phagocytosis: A Role for CYP2J2 Deficiency in the Pathogenesis of Crohn’s Disease?

摘要: The epoxygenase CYP2J2 has an emerging role in inflammation and vascular biology. of phagocytosis is not known its regulation human inflammatory diseases poorly understood. Here we investigated the bacterial expression monocytes from healthy controls Crohns disease patients. anti-inflammatory peripheral blood monocytes. Bacterial LPS induced mRNA protein. arachidonic acid products 11,12-EET 14,15-EET inhibited TNFα release. THP-1 were transformed into macrophages by 48h incubation with phorbol 12-myristate 13-acetate. Epoxygenase inhibition using a non-selective inhibitor SKF525A or selective Compound 4, E. coli particle phagocytosis, which could be specifically reversed 11,12-EET. Moreover, reduced receptors CD11b CD68. also mediates L. monocytogenes phagocytosis. Similar, to bioparticle intracellular levels monocytogenes, co-incubation Disrupted clearance hallmark Crohn’s disease. Unlike control donors, patients showed no induction response coli. These results demonstrate that macrophages, implicates defect pathway may regulate