About: Targeting the Linear Ubiquitin Assembly Complex to Modulate the Host Response and Improve Influenza A Virus Induced Lung Injury

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About: Targeting the Linear Ubiquitin Assembly Complex to Modulate the Host Response and Improve Influenza A Virus Induced 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	Targeting the Linear Ubiquitin Assembly Complex to Modulate the Host Response and Improve Influenza A Virus Induced Lung Injury
Creator	Sznajder, Jacob Brazee, Patricia Superior, E
Source	Elsevier; Medline; PMC
abstract	Abstract Influenza virus infection is characterized by symptoms ranging from mild congestion and body aches to severe pulmonary edema and respiratory failure. While the majority of those exposed have minor symptoms and recover with little morbidity, an estimated 500,000 people succumb to IAV-related complications each year worldwide. In these severe cases, an exaggerated inflammatory response, known as “cytokine storm”, occurs which results in damage to the respiratory epithelial barrier and development of acute respiratory distress syndrome (ARDS). Data from retrospective human studies as well as experimental animal models of influenza virus infection highlight the fine line between an excessive and an inadequate immune response, where the host response must balance viral clearance with exuberant inflammation. Current pharmacological modulators of inflammation, including corticosteroids and statins, have not been successful in improving outcomes during influenza virus infection. We have reported that the amplitude of the inflammatory response is regulated by Linear Ubiquitin Assembly Complex (LUBAC) activity and that dampening of LUBAC activity is protective during severe influenza virus infection. Therapeutic modulation of LUBAC activity may be crucial to improve outcomes during severe influenza virus infection, as it functions as a molecular rheostat of the host response. Here we review the evidence for modulating inflammation to ameliorate influenza virus infection-induced lung injury, data on current anti-inflammatory strategies, and potential new avenues to target viral inflammation and improve outcomes.
has issue date	2020-05-13(xsd:dateTime)
bibo:doi	10.1016/j.arbres.2020.04.019
bibo:pmid	32405132
has license	els-covid
sha1sum (hex)	c0b85e7f8627c38dda91271859949d131bbc0ae1
schema:url	https://doi.org/10.1016/j.arbres.2020.04.019
resource representing a document's title	Targeting the Linear Ubiquitin Assembly Complex to Modulate the Host Response and Improve Influenza A Virus Induced Lung Injury
has PubMed Central identifier	PMC7218391
has PubMed identifier	32405132
schema:publication	Arch Bronconeumol
resource representing a document's body	covid:c0b85e7f8627c38dda91271859949d131bbc0ae1#body_text
is schema:about of	named entity 'While' named entity 'Influenza A' named entity 'SYMPTOMS' named entity 'MINOR' named entity 'SEVERE' named entity 'RECOVER' named entity 'YEAR' named entity 'RESPIRATORY FAILURE' named entity 'MILD' named entity 'pulmonary edema' named entity 'aches' named entity 'majority' named entity 'Influenza virus' named entity 'morbidity' named entity 'congestion' named entity 'Linear' named entity 'Improve' named entity 'pulmonary edema' named entity 'Lung Injury' named entity 'epithelial cells' named entity 'inflammation' named entity 'protein' named entity 'host response' named entity 'gliotoxin' named entity 'virulence' named entity 'HOIP' named entity 'macrophages' named entity 'ubiquitin' named entity 'cytokines' named entity 'infection' named entity 'HOIP' named entity 'infection' named entity 'IAV' named entity 'viral infection' named entity 'protein' named entity 'ARDS' named entity 'cytokine storm' named entity 'bacterial sepsis' named entity 'chemical reaction' named entity 'pandemic strains' named entity 'lung' named entity 'observational studies' named entity 'viral infections' named entity 'IAV' named entity 'inflammation' named entity 'antiviral drugs' named entity 'IκB' named entity 'phosphorylation' named entity 'inflammatory response' named entity 'infection' named entity 'infection' named entity 'IAV' named entity 'IAV' named entity 'gliotoxin' named entity 'rheostat' named entity 'IκBα' named entity 'NF-κB' named entity 'anti-inflammatory' named entity 'innate immunity' named entity 'E3 ubiquitin ligase' named entity 'influenza' named entity 'respiratory epithelium' named entity 'catalytic site' named entity 'vaccination' named entity 'anti-inflammatory drugs' named entity 'FDA' named entity 'viral infection' named entity 'cytotoxicity' named entity 'Seasonal influenza' named entity 'anti-viral drugs' named entity 'host response' named entity 'statins' named entity 'IAV' named entity 'Gliotoxin' named entity 'seasonal influenza' named entity 'HOIP' named entity 'infection' named entity 'NK cells' named entity 'NF-kB'

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