About: IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis

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About: IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis 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	IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis
Creator	Chen, Tao Weng, Dong Wu, Qin Chen, Shan-Shan Li, \| Meng, \| Dong, \| Li, Hui-Ping Lu, -Qin Qiu, \| Song, Jia-Cui Tang, Dan-Li Zhao, Meng Zhou, Nian-Yu
Source	Medline; PMC
abstract	BACKGROUND: Patients with idiopathic pulmonary fibrosis (IPF) often experience acute exacerbation (AE) after an episode of common cold. AIMS: To establish a mouse model of virus infection‐induced AE‐IPF and investigate the mechanism underlying the AE‐IPF. METHODS: Herpes simplex virus 1 (HSV1) was inoculated intranasally to wild‐type (WT) and IL‐17A gene knockout (IL‐17A(‐/‐)) mice 21 days after intratracheal administration of bleomycin (BLM). RESULTS: HSV1 infection caused acute exacerbation in mice with BLM‐induced fibrosis. Compared with the BLM+Saline mice, the mice with BLM+HSV1 showed significantly higher acute lung injury (ALI) score (P < 0.0001), lower survival rate (100% vs 21.4%, P < 0.0001), poorer lung function and higher inflammatory response representing by increased total inflammatory cells in bronchoalveolar lavage fluid (BALF) (P = 0.0323), increased proportion of Th17 cells in peripheral blood (P = 0.0004) and higher inflammatory factors in BALF. In addition, HSV1 infection increased the expression of endoplasmic reticulum stress (ERS)‐related proteins in mice with BLM‐induced fibrosis. The inhibition of ERS by tauroursodeoxycholic acid (TUDCA, an ERS inhibitor) significantly reduced the IL‐17A levels in BALF (P = 0.0140) and TH17 cells in the peripheral blood (P = 0.0084) of mice with BLM+HSV1, suggesting that suppression of ERS may reduce TH17 response in mice with AE‐IPF. Compared with WT mice with BLM+HSV1, IL‐17A(‐/‐) mice with BLM+HSV1 had lower ALI score (P = 0.0119), higher survival rate (78.6% vs 21.4%, P = 0.004), improved lung function, and milder inflammatory response. CONCLUSIONS: HSV1 infection in addition to BLM‐induced IPF can successfully establish AE‐IPF in mice. IL‐17A and ERS promote lung inflammation in AE‐IPF development.
has issue date	2018-10-30(xsd:dateTime)
bibo:doi	10.1111/jcmm.13992
bibo:pmid	30378252
has license	cc-by
sha1sum (hex)	937d7695ba3f5f31a54eef142d6865c6460d5032
schema:url	https://doi.org/10.1111/jcmm.13992
resource representing a document's title	IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis
has PubMed Central identifier	PMC6349191
has PubMed identifier	30378252
schema:publication	J Cell Mol Med
resource representing a document's body	covid:937d7695ba3f5f31a54eef142d6865c6460d5032#body_text
is schema:about of	named entity 'IL-17A' named entity 'mice' named entity 'Methods' named entity 'expression' named entity 'ALI' named entity 'episode' named entity 'HSV1' named entity 'score' named entity 'ERS' named entity 'common cold' named entity 'fibrosis' named entity 'HSV1' named entity 'IL-17A' named entity 'MOUSE MODEL' named entity 'PATIENTS' named entity 'TH17 CELLS' named entity 'IL-17A GENE' named entity 'BRONCHOALVEOLAR LAVAGE FLUID' named entity 'PROTEINS' named entity 'LEVELS' named entity 'SURVIVAL RATE' named entity 'HSV1' named entity 'MODEL OF' named entity 'IMPROVED' named entity 'SUPPRESSION' named entity 'FIBROSIS' named entity 'INTRATRACHEAL ADMINISTRATION' named entity 'TOTAL' named entity 'ERS' named entity 'A MOUSE' named entity 'INFECTION' named entity '28P' named entity 'MECHANISM' named entity 'DAYS' named entity 'PULMONARY FIBROSIS' named entity 'INTERLEUKIN-17A' named entity 'INFLAMMATORY RESPONSE' named entity 'REDUCED' named entity 'COMPARED' named entity 'TH17' named entity 'BACKGROUND' named entity 'BLM' named entity 'METHODS' named entity 'LUNG FUNCTION' named entity 'HIGHER' named entity 'GENE KNOCKOUT' named entity 'INVESTIGATE' named entity 'EPISODE OF' named entity 'ESTABLISH' named entity 'DEVELOPMENT' named entity '17A' named entity 'RESULTS' named entity 'MOUSE MODEL' named entity 'BLEOMYCIN' named entity 'EXPERIENCE' named entity 'MICE' named entity 'UNDERLYING' named entity 'CHEN' named entity 'INDUCED' named entity 'RELATED' named entity 'SCORE' named entity '28100' named entity 'R D' named entity 'IPF' named entity 'RESPONSE' named entity 'INHIBITOR' named entity 'HUI' named entity 'BY INCREASED'

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