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The mito-DAMP cardiolipin blocks IL-10 production causing persistent inflammation during bacterial pneumonia.
Chakraborty, Krishnendu; Raundhal, Mahesh; Chen, Bill B; Morse, Christina; Tyurina, Yulia Y; Khare, Anupriya; Oriss, Timothy B; Huff, Rachael; Lee, Janet S; St Croix, Claudette M; Watkins, Simon; Mallampalli, Rama K; Kagan, Valerian E; Ray, Anuradha; Ray, Prabir.
Afiliación
  • Chakraborty K; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  • Raundhal M; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  • Chen BB; Department of Immunology, 200 Lothrop St, University of Pittsburgh School of Medicine, E1040 BSTWR, Pittsburgh, Pennsylvania 15261, USA.
  • Morse C; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  • Tyurina YY; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  • Khare A; Center for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, University of Pittsburgh School of Medicine, Bridgeside Point, 100 Technology Drive, Suite 350, Pittsburgh, Pennsylvania 15219, USA.
  • Oriss TB; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  • Huff R; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  • Lee JS; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  • St Croix CM; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  • Watkins S; Center for Biologic Imaging, University of Pittsburgh School of Medicine, 3500 Terrace St, Pittsburgh, Pennsylvania 15261, USA.
  • Mallampalli RK; Center for Biologic Imaging, University of Pittsburgh School of Medicine, 3500 Terrace St, Pittsburgh, Pennsylvania 15261, USA.
  • Kagan VE; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  • Ray A; Center for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, University of Pittsburgh School of Medicine, Bridgeside Point, 100 Technology Drive, Suite 350, Pittsburgh, Pennsylvania 15219, USA.
  • Ray P; Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
Nat Commun ; 8: 13944, 2017 01 11.
Article en En | MEDLINE | ID: mdl-28074841
Bacterial pneumonia is a significant healthcare burden worldwide. Failure to resolve inflammation after infection precipitates lung injury and an increase in morbidity and mortality. Gram-negative bacteria are common in pneumonia and increased levels of the mito-damage-associated molecular pattern (DAMP) cardiolipin can be detected in the lungs. Here we show that mice infected with Klebsiella pneumoniae develop lung injury with accumulation of cardiolipin. Cardiolipin inhibits resolution of inflammation by suppressing production of anti-inflammatory IL-10 by lung CD11b+Ly6GintLy6CloF4/80+ cells. Cardiolipin induces PPARγ SUMOylation, which causes recruitment of a repressive NCOR/HDAC3 complex to the IL-10 promoter, but not the TNF promoter, thereby tipping the balance towards inflammation rather than resolution. Inhibition of HDAC activity by sodium butyrate enhances recruitment of acetylated histone 3 to the IL-10 promoter and increases the concentration of IL-10 in the lungs. These findings identify a mechanism of persistent inflammation during pneumonia and indicate the potential of HDAC inhibition as a therapy.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones por Klebsiella / Cardiolipinas / Interleucina-10 / Neumonía Bacteriana / Inflamación / Klebsiella pneumoniae Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Nat Commun Asunto de la revista: BIOLOGIA / CIENCIA Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones por Klebsiella / Cardiolipinas / Interleucina-10 / Neumonía Bacteriana / Inflamación / Klebsiella pneumoniae Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Nat Commun Asunto de la revista: BIOLOGIA / CIENCIA Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido