title: Reduced apoptosis and ameliorated listeriosis in TRAIL-null mice.
abstract: Listeriosis is an infectious disease caused by the bacterium Listeria monocytogenes. Although it is well recognized that apoptosis plays a critical role in the pathogenesis of the disease, the molecular mechanisms of cell death in listeriosis remain to be established. We report in this study that mice deficient in TRAIL were partially resistant to primary listeriosis, and blocking TRAIL with a soluble death receptor 5 markedly ameliorated the disease. The numbers of Listeria in the liver and spleen of TRAIL+/+ mice were 10-100 times greater than those in TRAIL-/- mice following primary Listeria infection. This was accompanied by a significant increase in the survival rate of TRAIL-/- mice. Lymphoid and myeloid cell death was significantly inhibited in TRAIL-/- mice, which led to marked enlargement of the spleen. These results establish a critical role for TRAIL in apoptosis during listeriosis.
authors.affiliation: Department of Pathology, University of Pennsylvania, Philadelphia, PA 19104, USA.
authors.forename: Shi-Jun
authors.initials: SJ
authors.lastname: Zheng
authors.forename: Jiu
authors.initials: J
authors.lastname: Jiang
authors.forename: Hao
authors.initials: H
authors.lastname: Shen
authors.forename: Youhai H
authors.initials: YH
authors.lastname: Chen
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics* / Q000276:immunology*; D051017:Apoptosis Regulatory Proteins; D016923:Cell Death / Q000235:genetics / Q000276:immunology; D002470:Cell Survival / Q000235:genetics / Q000276:immunology; D007113:Immunity, Innate / Q000235:genetics; D008024:Ligands; D008089:Listeria monocytogenes / Q000276:immunology; D008088:Listeriosis / Q000235:genetics / Q000276:immunology / Q000473:pathology* / Q000517:prevention & control*; D008099:Liver / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D008212:Lymphocyte Depletion; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000172:deficiency* / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D022423:Myeloid Cells / Q000276:immunology / Q000473:pathology; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis / Q000502:physiology; D013154:Spleen / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D053221:TNF-Related Apoptosis-Inducing Ligand; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000172:deficiency* / Q000502:physiology; D015854:Up-Regulation / Q000235:genetics / Q000276:immunology
chemical_list: D051017:Apoptosis Regulatory Proteins; D008024:Ligands; D008562:Membrane Glycoproteins; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand; D018124:Receptors, Tumor Necrosis Factor; D053221:TNF-Related Apoptosis-Inducing Ligand; C505640:Tnfrsf10b protein, mouse; C505654:Tnfsf10 protein, mouse; D014409:Tumor Necrosis Factor-alpha