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Identification of oxidative stress and toll-like receptor 4 signaling as a key pathway of acute lung injury

Yumiko Imai, Keiji Kuba, G Greg Neely, Rubina Yaghubian-Malhami, Thomas Perkmann, Geert van Loo UGent, Maria Ermolaeva, Ruud Veldhuizen, YH Connie Leung and Hongliang Wang, et al. (2008) CELL. 133(2). p.235-249
abstract
Multiple lung pathogens such as chemical agents, H5N1 avian flu, or SARS cause high lethality due to acute respiratory distress syndrome. Here we report that Toll-like receptor 4 (TLR4) mutant mice display natural resistance to acid-induced acute lung injury (ALI). We show that TLR4-TRIF-TRAF6 signaling is a key disease pathway that controls the severity of ALI. The oxidized phospholipid (OxPL) OxPAPC was identified to induce lung injury and cytokine production by lung macrophages via TLR4-TRIF. We observed OxPL production in the lungs of humans and animals infected with SARS, Anthrax, or H5N1. Pulmonary challenge with an inactivated H5N1 avian influenza virus rapidly induces ALI and OxPL formation in mice. Loss of TLR4 or TRIF expression protects mice from H5N1-induced ALI. Moreover, deletion of ncf1, which controls ROS production, improves the severity of H5N1-mediated ALI. Our data identify oxidative stress and innate immunity as key lung injury pathways that control the severity of ALI.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
APOPTOTIC CELLS, SYNCYTIAL VIRUS, APOLIPOPROTEIN-E, PULMONARY SURFACTANT, FACTOR-KAPPA-B, 1918 PANDEMIC VIRUS, LOW-DENSITY-LIPOPROTEIN, RESPIRATORY-DISTRESS-SYNDROME, TRANSCRIPTION FACTORS, OXIDIZED PHOSPHOLIPIDS
journal title
CELL
Cell
volume
133
issue
2
pages
235 - 249
Web of Science type
Article
Web of Science id
000255052000014
JCR category
CELL BIOLOGY
JCR impact factor
31.253 (2008)
JCR rank
3/157 (2008)
JCR quartile
1 (2008)
ISSN
0092-8674
DOI
10.1016/j.cell.2008.02.043
language
English
UGent publication?
no
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2976377
handle
http://hdl.handle.net/1854/LU-2976377
date created
2012-08-29 13:23:06
date last changed
2012-09-06 10:23:23
@article{2976377,
  abstract     = {Multiple lung pathogens such as chemical agents, H5N1 avian flu, or SARS cause high lethality due to acute respiratory distress syndrome. Here we report that Toll-like receptor 4 (TLR4) mutant mice display natural resistance to acid-induced acute lung injury (ALI). We show that TLR4-TRIF-TRAF6 signaling is a key disease pathway that controls the severity of ALI. The oxidized phospholipid (OxPL) OxPAPC was identified to induce lung injury and cytokine production by lung macrophages via TLR4-TRIF. We observed OxPL production in the lungs of humans and animals infected with SARS, Anthrax, or H5N1. Pulmonary challenge with an inactivated H5N1 avian influenza virus rapidly induces ALI and OxPL formation in mice. Loss of TLR4 or TRIF expression protects mice from H5N1-induced ALI. Moreover, deletion of ncf1, which controls ROS production, improves the severity of H5N1-mediated ALI. Our data identify oxidative stress and innate immunity as key lung injury pathways that control the severity of ALI.},
  author       = {Imai, Yumiko and Kuba, Keiji and Neely, G Greg and Yaghubian-Malhami, Rubina and Perkmann, Thomas and van Loo, Geert and Ermolaeva, Maria and Veldhuizen, Ruud and Leung, YH Connie and Wang, Hongliang and Liu, Haolin and Sun, Yang and Pasparakis, Manolis and Kopf, Manfred and Mech, Christin and Bavari, Sina and Peiris, JS Malik and Slutsky, Arthur S and Akira, Shizuo and Hultqvist, Malin and Holmdahl, Rikard and Nicholls, John and Jiang, Chengyu and Binder, Christoph J and Penninger, Josef M},
  issn         = {0092-8674},
  journal      = {CELL},
  keyword      = {APOPTOTIC CELLS,SYNCYTIAL VIRUS,APOLIPOPROTEIN-E,PULMONARY SURFACTANT,FACTOR-KAPPA-B,1918 PANDEMIC VIRUS,LOW-DENSITY-LIPOPROTEIN,RESPIRATORY-DISTRESS-SYNDROME,TRANSCRIPTION FACTORS,OXIDIZED PHOSPHOLIPIDS},
  language     = {eng},
  number       = {2},
  pages        = {235--249},
  title        = {Identification of oxidative stress and toll-like receptor 4 signaling as a key pathway of acute lung injury},
  url          = {http://dx.doi.org/10.1016/j.cell.2008.02.043},
  volume       = {133},
  year         = {2008},
}

Chicago
Imai, Yumiko, Keiji Kuba, G Greg Neely, Rubina Yaghubian-Malhami, Thomas Perkmann, Geert van Loo, Maria Ermolaeva, et al. 2008. “Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury.” Cell 133 (2): 235–249.
APA
Imai, Y., Kuba, K., Neely, G. G., Yaghubian-Malhami, R., Perkmann, T., van Loo, G., Ermolaeva, M., et al. (2008). Identification of oxidative stress and toll-like receptor 4 signaling as a key pathway of acute lung injury. CELL, 133(2), 235–249.
Vancouver
1.
Imai Y, Kuba K, Neely GG, Yaghubian-Malhami R, Perkmann T, van Loo G, et al. Identification of oxidative stress and toll-like receptor 4 signaling as a key pathway of acute lung injury. CELL. 2008;133(2):235–49.
MLA
Imai, Yumiko, Keiji Kuba, G Greg Neely, et al. “Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury.” CELL 133.2 (2008): 235–249. Print.