About: Excessive Neutrophils and Neutrophil Extracellular Traps Contribute to Acute Lung Injury of Influenza Pneumonitis

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

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Excessive Neutrophils and Neutrophil Extracellular Traps Contribute to Acute Lung Injury of Influenza Pneumonitis
Creator	Van Rooijen, Nico Liew, Audrey-Ann Narasaraju, Teluguakula Yang, Edwin Chee, Meng Chow, Vincent Ng, Huey Poh, Wee Samy, Ramar
Source	Elsevier; Medline; PMC
abstract	Complications of acute respiratory distress syndrome (ARDS) are common among critically ill patients infected with highly pathogenic influenza viruses. Macrophages and neutrophils constitute the majority of cells recruited into infected lungs, and are associated with immunopathology in influenza pneumonia. We examined pathological manifestations in models of macrophage- or neutrophil-depleted mice challenged with sublethal doses of influenza A virus H1N1 strain PR8. Infected mice depleted of macrophages displayed excessive neutrophilic infiltration, alveolar damage, and increased viral load, later progressing into ARDS-like pathological signs with diffuse alveolar damage, pulmonary edema, hemorrhage, and hypoxemia. In contrast, neutrophil-depleted animals showed mild pathology in lungs. The brochoalveolar lavage fluid of infected macrophage-depleted mice exhibited elevated protein content, T1-α, thrombomodulin, matrix metalloproteinase-9, and myeloperoxidase activities indicating augmented alveolar-capillary damage, compared to neutrophil-depleted animals. We provide evidence for the formation of neutrophil extracellular traps (NETs), entangled with alveoli in areas of tissue injury, suggesting their potential link with lung damage. When co-incubated with infected alveolar epithelial cells in vitro, neutrophils from infected lungs strongly induced NETs generation, and augmented endothelial damage. NETs induction was abrogated by anti-myeloperoxidase antibody and an inhibitor of superoxide dismutase, thus implying that NETs generation is induced by redox enzymes in influenza pneumonia. These findings support the pathogenic effects of excessive neutrophils in acute lung injury of influenza pneumonia by instigating alveolar-capillary damage.
has issue date	2011-07-01(xsd:dateTime)
bibo:doi	10.1016/j.ajpath.2011.03.013
bibo:pmid	21703402
has license	hybrid-oa
sha1sum (hex)	46ee2266b2315dd11276c4ba0e338468461bb928
schema:url	https://doi.org/10.1016/j.ajpath.2011.03.013
resource representing a document's title	Excessive Neutrophils and Neutrophil Extracellular Traps Contribute to Acute Lung Injury of Influenza Pneumonitis
has PubMed Central identifier	PMC3123873
has PubMed identifier	21703402
schema:publication	The American Journal of Pathology
resource representing a document's body	covid:46ee2266b2315dd11276c4ba0e338468461bb928#body_text
is schema:about of	named entity 'INFECTIOUS DISEASES' named entity 'COMPARED' named entity 'COMMON' named entity 'INCREASED' named entity 'INFECTED' named entity 'GENERATION' named entity 'PULMONARY EDEMA' named entity 'THROMBOMODULIN' named entity 'MANIFESTATIONS' named entity 'POTENTIAL' named entity 'HEMORRHAGE' named entity 'CONTRAST' named entity 'PR8' named entity 'COMPLICATIONS' named entity 'NETS' named entity 'INDICATING' named entity 'DOSES' named entity 'TISSUE INJURY' named entity 'MACROPHAGE' named entity 'LIKE' named entity 'NEUTROPHILS' named entity 'MICE' named entity 'CELLS' named entity 'ALVEOLAR DAMAGE' named entity 'INHIBITOR' named entity 'SUPEROXIDE DISMUTASE' named entity 'AREAS' named entity 'EXAMINED' named entity 'EVIDENCE FOR' named entity 'IN VITRO' named entity 'PATHOLOGICAL' named entity 'INDUCTION' named entity 'ALVEOLAR EPITHELIAL CELLS' named entity 'CRITICALLY ILL' named entity 'HIGHLY' named entity 'LUNGS' named entity 'STRAIN' named entity 'MYELOPEROXIDASE ANTIBODY' named entity 'MODELS' named entity 'ACTIVITIES' named entity 'IMMUNOPATHOLOGY' named entity 'THEIR' named entity 'LATER' named entity 'H1N1' named entity 'DEPLETED' named entity 'INCUBATED' named entity 'ASSOCIATED WITH' named entity 'PATHOLOGY' named entity 'MAJORITY' named entity 'NEUTROPHIL' named entity 'MYELOPEROXIDASE' named entity 'ACUTE RESPIRATORY DISTRESS SYNDROME' named entity '90%' named entity 'DISPLAYED' named entity 'LAVAGE FLUID' named entity 'SIGNS' named entity 'DAMAGE' named entity 'NEUTROPHILIC' named entity 'VIRAL LOAD' named entity 'CONTRIBUTE ' named entity 'EXCESSIVE' named entity 'NEUTROPHILS' named entity 'ACUTE LUNG INJURY' named entity 'INFLUENZA' named entity 'EXTRACELLULAR TRAPS' named entity 'PNEUMONITIS' named entity 'INFILTRATION' named entity 'PROGRESSING' named entity 'EXCESSIVE' named entity 'INFLUENZA VIRUSES' named entity 'ELEVATED PROTEIN' named entity 'MATRIX METALLOPROTEINASE-9' named entity 'LINK'

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