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Contribution of neutrophil-derived myeloperoxidase in the early phase of fulminant acute respiratory distress syndrome induced by influenza virus infection.
Microbiol Immunol. 2012 Mar; 56(3):171-82.MI

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 tight junctions, and formation of hyaline membranes. In addition to interferon (IFN)-α, plenty of keratinocyte-derived chemokines (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. The present study suggests that MPO-mediated OCl(-) generation affects claudin molecules and leads to protein leakage and viral spread as a damage factor in influenza-induced ARDS.

Authors+Show Affiliations

Inflammation Program, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-city, Chiba 260-8670, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22211924

Citation

Sugamata, Ryuichi, et al. "Contribution of Neutrophil-derived Myeloperoxidase in the Early Phase of Fulminant Acute Respiratory Distress Syndrome Induced By Influenza Virus Infection." Microbiology and Immunology, vol. 56, no. 3, 2012, pp. 171-82.
Sugamata R, Dobashi H, Nagao T, et al. Contribution of neutrophil-derived myeloperoxidase in the early phase of fulminant acute respiratory distress syndrome induced by influenza virus infection. Microbiol Immunol. 2012;56(3):171-82.
Sugamata, R., Dobashi, H., Nagao, T., Yamamoto, K., Nakajima, N., Sato, Y., Aratani, Y., Oshima, M., Sata, T., Kobayashi, K., Kawachi, S., Nakayama, T., & Suzuki, K. (2012). Contribution of neutrophil-derived myeloperoxidase in the early phase of fulminant acute respiratory distress syndrome induced by influenza virus infection. Microbiology and Immunology, 56(3), 171-82. https://doi.org/10.1111/j.1348-0421.2011.00424.x
Sugamata R, et al. Contribution of Neutrophil-derived Myeloperoxidase in the Early Phase of Fulminant Acute Respiratory Distress Syndrome Induced By Influenza Virus Infection. Microbiol Immunol. 2012;56(3):171-82. PubMed PMID: 22211924.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Contribution of neutrophil-derived myeloperoxidase in the early phase of fulminant acute respiratory distress syndrome induced by influenza virus infection. AU - Sugamata,Ryuichi, AU - Dobashi,Hideki, AU - Nagao,Tomokazu, AU - Yamamoto,Ki-Ichi, AU - Nakajima,Noriko, AU - Sato,Yuko, AU - Aratani,Yasuaki, AU - Oshima,Masamichi, AU - Sata,Tetsutaro, AU - Kobayashi,Kazuo, AU - Kawachi,Shoji, AU - Nakayama,Toshinori, AU - Suzuki,Kazuo, PY - 2012/1/4/entrez PY - 2012/1/4/pubmed PY - 2012/7/25/medline SP - 171 EP - 82 JF - Microbiology and immunology JO - Microbiol Immunol VL - 56 IS - 3 N2 - 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 tight junctions, and formation of hyaline membranes. In addition to interferon (IFN)-α, plenty of keratinocyte-derived chemokines (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. The present study suggests that MPO-mediated OCl(-) generation affects claudin molecules and leads to protein leakage and viral spread as a damage factor in influenza-induced ARDS. SN - 1348-0421 UR - https://www.unboundmedicine.com/medline/citation/22211924/Contribution_of_neutrophil_derived_myeloperoxidase_in_the_early_phase_of_fulminant_acute_respiratory_distress_syndrome_induced_by_influenza_virus_infection_ L2 - https://doi.org/10.1111/j.1348-0421.2011.00424.x DB - PRIME DP - Unbound Medicine ER -