tetano
Editor, Senior Moderator
Microbiol Immunol. 2011 Dec 30. doi: 10.1111/j.1348-0421.2011.00424.x. [Epub ahead of print]
The contribution of neutrophil-derived myeloperoxidase in the early phase of fulminant acute respiratory distress syndrome induced by influenza virus infection.
Sugamata R, Dobashi H, Nagao T, Yamamoto KI, Nakajima N, Sato Y, Aratani Y, Oshima M, Sata T, Kobayashi K, Kawachi S, Nakayama T, Suzuki K.
Source
Inflammation Program, Department of Immunology, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-city, Chiba 260-8670 Japan Departments of Immunology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan Departments of Pathology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan Graduate School of Nanobioscience, Yokohama City University, Seto 22-2, Kanazawa-ku, Yokohama-city, Kanagawa 236-0027, Japan Division of Anesthesia, Surgical Operation Department, National Center for Global Health and Medicine, Toyama 1-21-1, Shinjuku-ku, Tokyo 162-8655, Japan. Department of Immunology, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-city, Chiba 260-8670 Japan.
Abstract
Because the pathogenesis of acute respiratory distress syndrome (ARDS) induced by influenza virus infection remains unknown, we can only improve on existing therapeutic interventions. To approach the subject, we investigated immunological etiology focused on cytokines and an acute lung damage factor in influenza-induced ARDS by using a PR-8 (A/H1N1)-infected mouse model. The infected mouse showed fulminant severe pneumonia with leukocyte infiltration, claudin alteration on broncheolar epithelial tight junctions, and formation of hyaline membranes. In addition to IFN-α, plenty of keratinocyte-derived chemokine (KC), macrophage inflammatory protein 2 (MIP-2), regulated on activation, normal T cell expressed and secreted (RANTES), and monocyte chemotactic protein 1 (MCP-1) were significantly released into bronchoalveolar lavage fluid (BALF) of the model. We focused on neutrophil myeloperoxidase (MPO) as a potent tissue damage factor and examined its contribution in influenza pneumonia by using mice genetically lacking in MPO. The absence of MPO reduced inflammatory damage with suppression of leakage of total BALF proteins associated with alteration of claudins in the lung. MPO(-/-) mice also suppressed viral load in the lung. This study suggests that MPO-mediated OCl(-) generation affects claudin molecules and leads to protein leakage and viral spread as a damage factor oin influenza-induced ARDS.
? 2011 The Societies and Blackwell Publishing Asia Pty Ltd.
PMID:
22211924
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22211924
The contribution of neutrophil-derived myeloperoxidase in the early phase of fulminant acute respiratory distress syndrome induced by influenza virus infection.
Sugamata R, Dobashi H, Nagao T, Yamamoto KI, Nakajima N, Sato Y, Aratani Y, Oshima M, Sata T, Kobayashi K, Kawachi S, Nakayama T, Suzuki K.
Source
Inflammation Program, Department of Immunology, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-city, Chiba 260-8670 Japan Departments of Immunology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan Departments of Pathology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan Graduate School of Nanobioscience, Yokohama City University, Seto 22-2, Kanazawa-ku, Yokohama-city, Kanagawa 236-0027, Japan Division of Anesthesia, Surgical Operation Department, National Center for Global Health and Medicine, Toyama 1-21-1, Shinjuku-ku, Tokyo 162-8655, Japan. Department of Immunology, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-city, Chiba 260-8670 Japan.
Abstract
Because the pathogenesis of acute respiratory distress syndrome (ARDS) induced by influenza virus infection remains unknown, we can only improve on existing therapeutic interventions. To approach the subject, we investigated immunological etiology focused on cytokines and an acute lung damage factor in influenza-induced ARDS by using a PR-8 (A/H1N1)-infected mouse model. The infected mouse showed fulminant severe pneumonia with leukocyte infiltration, claudin alteration on broncheolar epithelial tight junctions, and formation of hyaline membranes. In addition to IFN-α, plenty of keratinocyte-derived chemokine (KC), macrophage inflammatory protein 2 (MIP-2), regulated on activation, normal T cell expressed and secreted (RANTES), and monocyte chemotactic protein 1 (MCP-1) were significantly released into bronchoalveolar lavage fluid (BALF) of the model. We focused on neutrophil myeloperoxidase (MPO) as a potent tissue damage factor and examined its contribution in influenza pneumonia by using mice genetically lacking in MPO. The absence of MPO reduced inflammatory damage with suppression of leakage of total BALF proteins associated with alteration of claudins in the lung. MPO(-/-) mice also suppressed viral load in the lung. This study suggests that MPO-mediated OCl(-) generation affects claudin molecules and leads to protein leakage and viral spread as a damage factor oin influenza-induced ARDS.
? 2011 The Societies and Blackwell Publishing Asia Pty Ltd.
PMID:
22211924
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22211924