About: Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury

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About: Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury
Creator	Sun, Yang Imai, Yumiko Kuba, Keiji Jiang, Chengyu Bavari, Sina Akira, Shizuo Holmdahl, Rikard Hultqvist, Malin Liu, Haolin Wang, Hongliang Peiris, J Pasparakis, Manolis Ermolaeva, Maria Kopf, Manfred Mech, Christin Nicholls, John Perkmann, Thomas Veldhuizen, Ruud Yaghubian-Malhami, Rubina Binder, Christoph Penninger, Josef Slutsky, Arthur Leung, Y Neely, G Van Loo, Geert
Source	Elsevier; Medline; PMC
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.
has issue date	2008-04-18(xsd:dateTime)
bibo:doi	10.1016/j.cell.2008.02.043
bibo:pmid	18423196
has license	no-cc
sha1sum (hex)	378773f6c9d010ee15efbe438e3aa3161fe0745c
schema:url	https://doi.org/10.1016/j.cell.2008.02.043
resource representing a document's title	Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury
has PubMed Central identifier	PMC7112336
has PubMed identifier	18423196
schema:publication	Cell
resource representing a document's body	covid:378773f6c9d010ee15efbe438e3aa3161fe0745c#body_text
is schema:about of	named entity 'Our' named entity 'acute lung injury' named entity 'lung injury' named entity 'TLR4' named entity 'mediated' named entity 'expression' named entity 'natural' named entity 'disease' named entity 'Pathway' covid:arg/378773f6c9d010ee15efbe438e3aa3161fe0745c named entity 'induce' named entity 'avian influenza' named entity 'lung' named entity 'humans' named entity 'rapidly' named entity 'mutant' named entity 'key' named entity 'key' named entity 'Multiple' named entity 'production' named entity 'mice' named entity 'Loss' named entity 'TRIF' named entity 'lungs' named entity 'Injury' named entity 'ALI' named entity 'acid-induced' named entity 'oxidized' named entity 'avian influenza virus' named entity 'lung' named entity 'TRIF' named entity 'TLR4' named entity 'Toll-like receptor 4' named entity 'cytokine' named entity 'chemical agents' named entity 'ALI' named entity 'pathogens' named entity 'ALI' named entity 'macrophages' named entity 'mice' named entity 'LPS' named entity 'protein' named entity 'TLR4' named entity 'tlr4' named entity 'TLR4' named entity 'IL-6' named entity 'macrophages' named entity 'H5N1' named entity 'E. coli' named entity 'lipid peroxidation' named entity 'histology' named entity 'LPS' named entity 'tlr4' named entity 'mAb' named entity 'genetic deletion' named entity 'GM-CSF' named entity 'MyD88'

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