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About:
CHAC1 Is Differentially Expressed in Normal and Cystic Fibrosis Bronchial Epithelial Cells and Regulates the Inflammatory Response Induced by Pseudomonas aeruginosa
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covidontheweb.inria.fr
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Type:
Academic Article
research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
CHAC1 Is Differentially Expressed in Normal and Cystic Fibrosis Bronchial Epithelial Cells and Regulates the Inflammatory Response Induced by Pseudomonas aeruginosa
Creator
Hammerschmidt, Sven
Balloy, Viviane
Chignard, Michel
Corvol, Harriet
Foussignière, Tobias
Guillot, Loic
Moissenet, Didier
Perra, Léa
Petat, Hortense
Touqui, Lhousseine
Hilgendorff, Anne
Mungrue, Imran
Filep, Janos
Source
Medline; PMC
abstract
In cystic fibrosis (CF), Pseudomonas aeruginosa (Pa) colonizes the lungs, leading to chronic inflammation of the bronchial epithelium. ChaC glutathione-specific γ-glutamylcyclotransferase 1 (CHAC1) mRNA is differentially expressed in primary human airway epithelial cells from bronchi (hAECBs) from patients with CF and healthy patients at baseline and upon infection with Pa. CHAC1 degrades glutathione and is associated with ER stress and apoptosis pathways. In this study, we examined the roles of CHAC1 in the inflammatory response and apoptosis in lung epithelial cells. First, we confirmed by reverse transcription quantitative polymerase chain reaction that CHAC1 mRNA was overexpressed in hAECBs from patients without CF compared with the expression in hAECBs from patients with CF upon Pa (PAK strain) infection. Moreover, the Pa virulence factors LPS and flagellin were shown to induce CHAC1 expression in cells from patients without CF. Using NCI-H292 lung epithelial cells, we found that LPS-induced CHAC1 mRNA expression was PERK-independent and involved ATF4. Additionally, using CHAC1 small interfering RNA, we showed that reduced CHAC1 expression in the context of LPS and flagellin stimulation was associated with modulation of inflammatory markers and alteration of NF-κB signaling. Finally, we showed that Pa was not able to induce apoptosis in NCI-H292 cells. Our results suggest that CHAC1 is involved in the regulation of inflammation in bronchial cells during Pa infection and may explain the excessive inflammation present in the respiratory tracts of patients with CF.
has issue date
2018-11-29
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bibo:doi
10.3389/fimmu.2018.02823
bibo:pmid
30555487
has license
cc-by
sha1sum (hex)
dcfa47b076db144f586108d35f5d43e5100c02d5
schema:url
https://doi.org/10.3389/fimmu.2018.02823
resource representing a document's title
CHAC1 Is Differentially Expressed in Normal and Cystic Fibrosis Bronchial Epithelial Cells and Regulates the Inflammatory Response Induced by Pseudomonas aeruginosa
has PubMed Central identifier
PMC6282009
has PubMed identifier
30555487
schema:publication
Front Immunol
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covid:dcfa47b076db144f586108d35f5d43e5100c02d5#body_text
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schema:about
of
named entity 'Our'
named entity 'human'
named entity 'apoptosis'
named entity 'patients'
named entity 'cystic fibrosis'
named entity 'patients'
named entity 'inflammatory'
named entity 'strain'
named entity 'chain reaction'
named entity 'induce'
named entity 'Cells'
named entity 'Response'
named entity 'lung'
named entity 'modulation'
named entity 'First'
named entity 'flagellin'
named entity 'cells'
named entity 'mRNA'
named entity 'primary'
named entity 'cells'
named entity 'mRNA'
named entity 'Pseudomonas aeruginosa'
named entity 'LPS'
named entity 'inflammation'
named entity 'infection'
named entity 'bronchi'
named entity 'small interfering RNA'
named entity 'infection'
named entity 'cystic fibrosis'
named entity 'glutathione'
named entity 'apoptosis'
named entity 'inflammatory response'
named entity 'Differentially Expressed'
named entity 'Pseudomonas aeruginosa'
named entity 'molecule'
named entity 'flagellin'
named entity 'transfected'
named entity 'Glutathione'
named entity 'bacterial infection'
named entity 'centrifuged'
named entity 'NCI'
named entity 'staurosporine'
named entity 'FliC'
named entity 'staurosporine'
named entity 'laboratory strain'
named entity 'PERK'
named entity 'luciferase'
named entity 'epithelial'
named entity 'IL-6'
named entity 'siRNA'
named entity 'endogenous'
named entity 'specific role'
named entity 'flagellin'
named entity 'Merck Millipore'
named entity 'glutathione'
named entity 'flagellin'
named entity 'A549'
named entity 'antibiotics'
named entity 'epithelial cells'
named entity 'mRNA expression'
named entity 'immune response'
named entity 'ATF4'
named entity 'PERK'
named entity 'inflammation'
named entity 'virulence factors'
named entity 'apoptosis'
named entity 'RNA'
named entity 'inflammatory markers'
named entity 'CST'
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