PMID- 22211924
OWN - NLM
STAT- MEDLINE
DCOM- 20120724
LR  - 20201209
IS  - 1348-0421 (Electronic)
IS  - 0385-5600 (Linking)
VI  - 56
IP  - 3
DP  - 2012 Mar
TI  - Contribution of neutrophil-derived myeloperoxidase in the early phase of 
      fulminant acute respiratory distress syndrome induced by influenza virus 
      infection.
PG  - 171-82
LID - 10.1111/j.1348-0421.2011.00424.x [doi]
AB  - 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)-alpha, 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.
CI  - (c) 2012 The Societies and Blackwell Publishing Asia Pty Ltd.
FAU - Sugamata, Ryuichi
AU  - Sugamata R
AD  - Inflammation Program, Graduate School of Medicine, Chiba University, Inohana 
      1-8-1, Chuo-ku, Chiba-city, Chiba 260-8670, Japan.
FAU - Dobashi, Hideki
AU  - Dobashi H
FAU - Nagao, Tomokazu
AU  - Nagao T
FAU - Yamamoto, Ki-Ichi
AU  - Yamamoto K
FAU - Nakajima, Noriko
AU  - Nakajima N
FAU - Sato, Yuko
AU  - Sato Y
FAU - Aratani, Yasuaki
AU  - Aratani Y
FAU - Oshima, Masamichi
AU  - Oshima M
FAU - Sata, Tetsutaro
AU  - Sata T
FAU - Kobayashi, Kazuo
AU  - Kobayashi K
FAU - Kawachi, Shoji
AU  - Kawachi S
FAU - Nakayama, Toshinori
AU  - Nakayama T
FAU - Suzuki, Kazuo
AU  - Suzuki K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - Microbiol Immunol
JT  - Microbiology and immunology
JID - 7703966
RN  - 0 (Cytokines)
RN  - EC 1.11.1.7 (Peroxidase)
SB  - IM
MH  - Animals
MH  - Cytokines/metabolism
MH  - Female
MH  - Influenza A Virus, H1N1 Subtype/*pathogenicity
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Neutrophils/*immunology
MH  - Orthomyxoviridae Infections/*pathology
MH  - Peroxidase/deficiency/*metabolism
MH  - Pneumonia, Viral/pathology
MH  - Respiratory Distress Syndrome/*pathology
EDAT- 2012/01/04 06:00
MHDA- 2012/07/25 06:00
CRDT- 2012/01/04 06:00
PHST- 2012/01/04 06:00 [entrez]
PHST- 2012/01/04 06:00 [pubmed]
PHST- 2012/07/25 06:00 [medline]
AID - 10.1111/j.1348-0421.2011.00424.x [doi]
PST - ppublish
SO  - Microbiol Immunol. 2012 Mar;56(3):171-82. doi: 10.1111/j.1348-0421.2011.00424.x.