Influenza A virus induction of oxidative stress and MMP-9 is associated with severe lung pathology in a mouse model.
Identifieur interne : 001074 ( Main/Merge ); précédent : 001073; suivant : 001075Influenza A virus induction of oxidative stress and MMP-9 is associated with severe lung pathology in a mouse model.
Auteurs : Yu-Hsiang Lee [Taïwan] ; Chia-Lin Lai ; Chai-Lin Lai ; Shih-Hung Hsieh ; Chi-Chang Shieh ; Li-Min Huang ; Betty A. Wu-HsiehSource :
- Virus research [ 1872-7492 ] ; 2013.
Descripteurs français
- KwdFr :
- Animaux, Espèces réactives de l'azote (métabolisme), Espèces réactives de l'oxygène (métabolisme), Infections à Orthomyxoviridae (anatomopathologie), Infections à Orthomyxoviridae (virologie), Interactions hôte-pathogène, Matrix metalloproteinase 9 (métabolisme), Modèles animaux de maladie humaine, Poumon (anatomopathologie), Souris, Souris de lignée C57BL, Sous-type H1N1 du virus de la grippe A (immunologie), Sous-type H1N1 du virus de la grippe A (pathogénicité), Sous-type H3N2 du virus de la grippe A (immunologie), Sous-type H3N2 du virus de la grippe A (pathogénicité), Stress oxydatif.
- MESH :
- anatomopathologie : Infections à Orthomyxoviridae, Poumon.
- immunologie : Sous-type H1N1 du virus de la grippe A, Sous-type H3N2 du virus de la grippe A.
- métabolisme : Espèces réactives de l'azote, Espèces réactives de l'oxygène, Matrix metalloproteinase 9.
- pathogénicité : Sous-type H1N1 du virus de la grippe A, Sous-type H3N2 du virus de la grippe A.
- virologie : Infections à Orthomyxoviridae.
- Animaux, Interactions hôte-pathogène, Modèles animaux de maladie humaine, Souris, Souris de lignée C57BL, Stress oxydatif.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, Host-Pathogen Interactions, Influenza A Virus, H1N1 Subtype (immunology), Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza A Virus, H3N2 Subtype (immunology), Influenza A Virus, H3N2 Subtype (pathogenicity), Lung (pathology), Matrix Metalloproteinase 9 (metabolism), Mice, Mice, Inbred C57BL, Orthomyxoviridae Infections (pathology), Orthomyxoviridae Infections (virology), Oxidative Stress, Reactive Nitrogen Species (metabolism), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , metabolism : Matrix Metalloproteinase 9, Reactive Nitrogen Species, Reactive Oxygen Species.
- immunology : Influenza A Virus, H1N1 Subtype, Influenza A Virus, H3N2 Subtype.
- pathogenicity : Influenza A Virus, H1N1 Subtype, Influenza A Virus, H3N2 Subtype.
- pathology : Lung, Orthomyxoviridae Infections.
- virology : Orthomyxoviridae Infections.
- Animals, Disease Models, Animal, Host-Pathogen Interactions, Mice, Mice, Inbred C57BL, Oxidative Stress.
Abstract
Infection by different strains of influenza virus presents different pictures. Whether the pathogenicity of influenza virus is defined by the ability of the virus to induce differential immunopathological responses in the lungs still remains unclear. We compared the immunopathological response induced by influenza virus A/WSN/33 (H1N1) and that by A/Panama-like (H3N2) virus in C57BL/6 mice. WSN virus, in contrast to Panama-like virus, induced high mortality and severe lung pathology accompanied by massive Gr-1(+) and CD11b(+) cell infiltration and high levels of CXCL6/GCP-2, CCL2/MCP-1 and TIMP-1 production. Infection by WSN virus but not by Panama-like virus induced up-regulation of the active and latent forms of MMP-9 in the lungs and MMP-2/9 inhibitor partially reduced WSN virus-induced lung pathology. Both Gr-1(+) and CD11b(+) cells in WSN virus-infected lungs produced reactive oxygen and nitrogen species (ROS/RNS). While wild type mice infected by WSN virus had severe lung pathology and the presence of oxidized phospholipids and numerous MMP-9(+) cells in the lungs, ncf1 deficiency ablated their expression and manifested less lung pathology. Employing a pulmonary mouse model we demonstrated in this study that infection by virulent influenza virus is characterized by a heavy cellular infiltration, severe lung pathology which is accompanied by oxidative stress and MMP-9 production.
DOI: 10.1016/j.virusres.2013.09.011
PubMed: 24055463
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pubmed:24055463Le document en format XML
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Whether the pathogenicity of influenza virus is defined by the ability of the virus to induce differential immunopathological responses in the lungs still remains unclear. We compared the immunopathological response induced by influenza virus A/WSN/33 (H1N1) and that by A/Panama-like (H3N2) virus in C57BL/6 mice. WSN virus, in contrast to Panama-like virus, induced high mortality and severe lung pathology accompanied by massive Gr-1(+) and CD11b(+) cell infiltration and high levels of CXCL6/GCP-2, CCL2/MCP-1 and TIMP-1 production. Infection by WSN virus but not by Panama-like virus induced up-regulation of the active and latent forms of MMP-9 in the lungs and MMP-2/9 inhibitor partially reduced WSN virus-induced lung pathology. Both Gr-1(+) and CD11b(+) cells in WSN virus-infected lungs produced reactive oxygen and nitrogen species (ROS/RNS). While wild type mice infected by WSN virus had severe lung pathology and the presence of oxidized phospholipids and numerous MMP-9(+) cells in the lungs, ncf1 deficiency ablated their expression and manifested less lung pathology. Employing a pulmonary mouse model we demonstrated in this study that infection by virulent influenza virus is characterized by a heavy cellular infiltration, severe lung pathology which is accompanied by oxidative stress and MMP-9 production.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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