Your browser doesn't support javascript.
loading
Inflammasome-Independent Role for NLRP3 in Controlling Innate Antihelminth Immunity and Tissue Repair in the Lung.
Chenery, Alistair L; Alhallaf, Rafid; Agha, Zainab; Ajendra, Jesuthas; Parkinson, James E; Cooper, Martha M; Chan, Brian H K; Eichenberger, Ramon M; Dent, Lindsay A; Robertson, Avril A B; Kupz, Andreas; Brough, David; Loukas, Alex; Sutherland, Tara E; Allen, Judith E; Giacomin, Paul R.
Afiliación
  • Chenery AL; Wellcome Centre for Cell-Matrix Research, Manchester M13 9PT, United Kingdom.
  • Alhallaf R; Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, United Kingdom.
  • Agha Z; Lydia Becker Institute for Immunology and Infection, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, United Kingdom.
  • Ajendra J; Centre for Molecular Therapeutics, Australian Institute of Tropical Health and Medicine, James Cook University, Smithfield, Queensland 4878, Australia.
  • Parkinson JE; Centre for Molecular Therapeutics, Australian Institute of Tropical Health and Medicine, James Cook University, Smithfield, Queensland 4878, Australia.
  • Cooper MM; Wellcome Centre for Cell-Matrix Research, Manchester M13 9PT, United Kingdom.
  • Chan BHK; Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, United Kingdom.
  • Eichenberger RM; Lydia Becker Institute for Immunology and Infection, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, United Kingdom.
  • Dent LA; Wellcome Centre for Cell-Matrix Research, Manchester M13 9PT, United Kingdom.
  • Robertson AAB; Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, United Kingdom.
  • Kupz A; Lydia Becker Institute for Immunology and Infection, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, United Kingdom.
  • Brough D; Centre for Molecular Therapeutics, Australian Institute of Tropical Health and Medicine, James Cook University, Smithfield, Queensland 4878, Australia.
  • Loukas A; Wellcome Centre for Cell-Matrix Research, Manchester M13 9PT, United Kingdom.
  • Sutherland TE; Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, United Kingdom.
  • Allen JE; Lydia Becker Institute for Immunology and Infection, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, United Kingdom.
  • Giacomin PR; Centre for Molecular Therapeutics, Australian Institute of Tropical Health and Medicine, James Cook University, Smithfield, Queensland 4878, Australia.
J Immunol ; 203(10): 2724-2734, 2019 11 15.
Article en En | MEDLINE | ID: mdl-31586037
Alternatively activated macrophages are essential effector cells during type 2 immunity and tissue repair following helminth infections. We previously showed that Ym1, an alternative activation marker, can drive innate IL-1R-dependent neutrophil recruitment during infection with the lung-migrating nematode, Nippostrongylus brasiliensis, suggesting a potential role for the inflammasome in the IL-1-mediated innate response to infection. Although inflammasome proteins such as NLRP3 have important proinflammatory functions in macrophages, their role during type 2 responses and repair are less defined. We therefore infected Nlrp3 -/- mice with N. brasiliensis Unexpectedly, compared with wild-type (WT) mice, infected Nlrp3 -/- mice had increased neutrophilia and eosinophilia, correlating with enhanced worm killing but at the expense of increased tissue damage and delayed lung repair. Transcriptional profiling showed that infected Nlrp3 -/- mice exhibited elevated type 2 gene expression compared with WT mice. Notably, inflammasome activation was not evident early postinfection with N. brasiliensis, and in contrast to Nlrp3 -/- mice, antihelminth responses were unaffected in caspase-1/11-deficient or WT mice treated with the NLRP3-specific inhibitor MCC950. Together these data suggest that NLRP3 has a role in constraining lung neutrophilia, helminth killing, and type 2 immune responses in an inflammasome-independent manner.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones por Strongylida / Inflamasomas / Proteína con Dominio Pirina 3 de la Familia NLR / Enfermedades Pulmonares Parasitarias / Nippostrongylus Tipo de estudio: Etiology_studies Idioma: En Revista: J Immunol Año: 2019 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones por Strongylida / Inflamasomas / Proteína con Dominio Pirina 3 de la Familia NLR / Enfermedades Pulmonares Parasitarias / Nippostrongylus Tipo de estudio: Etiology_studies Idioma: En Revista: J Immunol Año: 2019 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Estados Unidos