TBK1/IKKε Negatively Regulate LPS-Induced Neutrophil Necroptosis and Lung Inflammation.
Journal
Shock (Augusta, Ga.)
ISSN: 1540-0514
Titre abrégé: Shock
Pays: United States
ID NLM: 9421564
Informations de publication
Date de publication:
01 03 2021
01 03 2021
Historique:
pubmed:
15
9
2020
medline:
14
1
2022
entrez:
14
9
2020
Statut:
ppublish
Résumé
Cell necroptosis, a form of regulated inflammatory cell death, is one of the mechanisms that controls cell release of inflammatory mediators from innate immune cells, such as polymorphonuclear neutrophils (PMNs), and critically regulates the progress of inflammation. Cell necroptosis features receptor-interacting protein (RIPK) 1 activation and necroptosome formation. This leads to loss of plasma membrane integrity, the release of cell contents into the extracellular space, and subsequent increased inflammation. Here, we report an intra-PMN mechanism of negative regulation of necroptosis mediated through TBK1/IKKε. Using an in vivo mouse model of intratracheal injection (i.t.) of LPS and in vitro LPS stimulation of mouse PMN, we found that LPS-TLR4 signaling in PMNs activates and phosphorylates TBK1 and IKKε, which in turn suppress LPS-induced formation of the RIPK1-RIPK3-MLKL (necrosome) complex. TBK1 dysfunction by knockdown or inhibitor significantly increases the phosphorylation of RIPK1 (∼67%), RIPK3 (∼68%), and MLKL (∼50%) and promotes RIPK1-RIPK3 and RIPK3-MLKL interactions and increases PMN necroptosis (∼83%) in response to LPS, with subsequent augmented lung inflammation. These findings suggest that the LPS-TLR4-TBK1 axis serves as a negative regulator for PMN necroptosis and might be a therapeutic target for modulating PMN death and inflammation.
Identifiants
pubmed: 32925605
pii: 00024382-202103000-00009
doi: 10.1097/SHK.0000000000001632
pmc: PMC8183424
mid: NIHMS1706037
doi:
Substances chimiques
Lipopolysaccharides
0
Tbk1 protein, mouse
EC 2.7.1.-
Protein Serine-Threonine Kinases
EC 2.7.11.1
I-kappa B Kinase
EC 2.7.11.10
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
338-348Subventions
Organisme : BLRD VA
ID : IK6 BX004211
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL076179
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL079669
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL139547
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM102146
Pays : United States
Organisme : BLRD VA
ID : I01 BX004838
Pays : United States
Organisme : BLRD VA
ID : I01 BX002729
Pays : United States
Informations de copyright
Copyright © 2020 by the Shock Society.
Déclaration de conflit d'intérêts
The authors report no conflicts of interest.
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