ATG16L2 inhibits NLRP3 inflammasome activation through promoting ATG5-12-16L1 complex assembly and autophagy.

Szczegóły
Abstrakt

Tytuł:: ATG16L2 inhibits NLRP3 inflammasome activation through promoting ATG5-12-16L1 complex assembly and autophagy.
Autorzy:: Wang D; Department of Gastrointestinal Surgery, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuan T; Department of Gastrointestinal Surgery, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Liu J; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wen Z; Department of Gastrointestinal Surgery, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shen Y; Department of Gastrointestinal Surgery, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Tang J; Department of Gastrointestinal Surgery, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wang Z; Department of Gastrointestinal Surgery, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wu X; Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Źródło:: European journal of immunology [Eur J Immunol] 2022 Aug; Vol. 52 (8), pp. 1321-1334. Date of Electronic Publication: 2022 Apr 28.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: <2005->: Weinheim : Wiley-VCH
Original Publication: Weinheim, Verlag Chemie GmbH.
MeSH Terms:: Autophagy-Related Protein 5*/genetics
Autophagy-Related Protein 5*/metabolism
Carrier Proteins*/genetics
Carrier Proteins*/metabolism
Inflammasomes*/metabolism
NLR Family, Pyrin Domain-Containing 3 Protein*/genetics
NLR Family, Pyrin Domain-Containing 3 Protein*/metabolism
Animals ; Autophagy ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout
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Contributed Indexing:: Keywords: ATG16L2; Autophagy; Colitis; Mitochondria; NLRP3
Substance Nomenclature:: 0 (Atg16L2 protein, mouse)
0 (Atg5 protein, mouse)
0 (Autophagy-Related Protein 5)
0 (Carrier Proteins)
0 (Inflammasomes)
0 (NLR Family, Pyrin Domain-Containing 3 Protein)
0 (Nlrp3 protein, mouse)
Entry Date(s):: Date Created: 20220415 Date Completed: 20220808 Latest Revision: 20220826
Update Code:: 20240105
DOI:: 10.1002/eji.202149764
PMID:: 35426127
: Czasopismo naukowe

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NLRP3 inflammasome activation is regulated by autophagy, a process tightly controlled by the ATG16L family proteins. However, the inside mechanisms remain elusive. Although the autophagy-related protein ATG16L1 has been well characterized, regulation and biological functions of its close homolog ATG16L2 still remain elusive. Here we report that ATG16L2 deficiency attenuates LPS-induced autophagy flux in macrophages through mediating ATG5-12-16L1 complex assembly. Importantly, NLRP3 inflammasome activation is elevated in ATG16L2-deficient macrophages, which also have defects in mitochondrial integrity and respiration. Finally, ATG16l2 knockout mice are more susceptible to DSS-induced intestinal damage, which can be ameliorated by inhibition of NLRP3. Collectively, our data demonstrate that ATG16L2 positively regulates autophagy and ATG16L2 could be a potential target for manipulating aberrant NLRP3 inflammasome activation induced inflammatory diseases.
(© 2022 Wiley-VCH GmbH.)

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