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Caspase-8 mediates caspase-1 processing and innate immune defense in response to bacterial blockade of NF-κB and MAPK signaling.
Philip, Naomi H; Dillon, Christopher P; Snyder, Annelise G; Fitzgerald, Patrick; Wynosky-Dolfi, Meghan A; Zwack, Erin E; Hu, Baofeng; Fitzgerald, Louise; Mauldin, Elizabeth A; Copenhaver, Alan M; Shin, Sunny; Wei, Lei; Parker, Matthew; Zhang, Jinghui; Oberst, Andrew; Green, Douglas R; Brodsky, Igor E.
Afiliación
  • Philip NH; Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104;Institute for Immunology and ibrodsky@vet.upenn.edu nphilip@mail.med.upenn.edu.
  • Dillon CP; Departments of Immunology and.
  • Snyder AG; Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104;
  • Fitzgerald P; Departments of Immunology and.
  • Wynosky-Dolfi MA; Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104;
  • Zwack EE; Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104;
  • Hu B; Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104;
  • Fitzgerald L; Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104;
  • Mauldin EA; Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104;
  • Copenhaver AM; Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104;
  • Shin S; Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104;
  • Wei L; Department of Biostatistics and Bioinformatics, Roswell Park Cancer Institute, Buffalo, NY 14263; and.
  • Parker M; Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105;
  • Zhang J; Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105;
  • Oberst A; Department of Immunology, University of Washington, Seattle, WA 98109.
  • Green DR; Departments of Immunology and.
  • Brodsky IE; Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104;Institute for Immunology and ibrodsky@vet.upenn.edu nphilip@mail.med.upenn.edu.
Proc Natl Acad Sci U S A ; 111(20): 7385-90, 2014 May 20.
Article en En | MEDLINE | ID: mdl-24799700
Toll-like receptor signaling and subsequent activation of NF-κB- and MAPK-dependent genes during infection play an important role in antimicrobial host defense. The YopJ protein of pathogenic Yersinia species inhibits NF-κB and MAPK signaling, resulting in blockade of NF-κB-dependent cytokine production and target cell death. Nevertheless, Yersinia infection induces inflammatory responses in vivo. Moreover, increasing the extent of YopJ-dependent cytotoxicity induced by Yersinia pestis and Yersinia pseudotuberculosis paradoxically leads to decreased virulence in vivo, suggesting that cell death promotes anti-Yersinia host defense. However, the specific pathways responsible for YopJ-induced cell death and how this cell death mediates immune defense against Yersinia remain poorly defined. YopJ activity induces processing of multiple caspases, including caspase-1, independently of inflammasome components or the adaptor protein ASC. Unexpectedly, caspase-1 activation in response to the activity of YopJ required caspase-8, receptor-interacting serine/threonine kinase 1 (RIPK1), and Fas-associated death domain (FADD), but not RIPK3. Furthermore, whereas RIPK3 deficiency did not affect YopJ-induced cell death or caspase-1 activation, deficiency of both RIPK3 and caspase-8 or FADD completely abrogated Yersinia-induced cell death and caspase-1 activation. Mice lacking RIPK3 and caspase-8 in their hematopoietic compartment showed extreme susceptibility to Yersinia and were deficient in monocyte and neutrophil-derived production of proinflammatory cytokines. Our data demonstrate for the first time to our knowledge that RIPK1, FADD, and caspase-8 are required for YopJ-induced cell death and caspase-1 activation and suggest that caspase-8-mediated cell death overrides blockade of immune signaling by YopJ to promote anti-Yersinia immune defense.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: FN-kappa B / Caspasa 1 / Sistema de Señalización de MAP Quinasas / Caspasa 8 / Inmunidad Innata Límite: Animals Idioma: En Revista: Proc Natl Acad Sci U S A Año: 2014 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: FN-kappa B / Caspasa 1 / Sistema de Señalización de MAP Quinasas / Caspasa 8 / Inmunidad Innata Límite: Animals Idioma: En Revista: Proc Natl Acad Sci U S A Año: 2014 Tipo del documento: Article Pais de publicación: Estados Unidos