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Tytuł pozycji:

Visceral adipose NLRP3 impairs cognition in obesity via IL-1R1 on CX3CR1+ cells.

Tytuł:
Visceral adipose NLRP3 impairs cognition in obesity via IL-1R1 on CX3CR1+ cells.
Autorzy:
Guo DH; Department of Neuroscience and Regenerative Medicine.
Yamamoto M; Department of Neuroscience and Regenerative Medicine.
Hernandez CM; Department of Pharmacology and Toxicology.
Khodadadi H; Department of Oral Biology, and.
Baban B; Department of Oral Biology, and.; Plastic Surgery Section, Department of Surgery, Medical College of Georgia, Augusta University, Augusta, Georgia, USA.
Stranahan AM; Department of Neuroscience and Regenerative Medicine.
Źródło:
The Journal of clinical investigation [J Clin Invest] 2020 Apr 01; Vol. 130 (4), pp. 1961-1976.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural
Język:
English
Imprint Name(s):
Publication: 1999- : Ann Arbor, MI : American Society for Clinical Investigation
Original Publication: New Haven [etc.] American Society for Clinical Investigation.
MeSH Terms:
Cognition*
CX3C Chemokine Receptor 1/*metabolism
Hippocampus/*metabolism
Intra-Abdominal Fat/*metabolism
NLR Family, Pyrin Domain-Containing 3 Protein/*metabolism
Obesity/*metabolism
Receptors, Interleukin-1 Type I/*metabolism
Animals ; CX3C Chemokine Receptor 1/genetics ; Hippocampus/pathology ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Intra-Abdominal Fat/pathology ; Intra-Abdominal Fat/transplantation ; Mice ; Mice, Knockout ; Microglia/metabolism ; Microglia/pathology ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Obesity/genetics ; Obesity/pathology ; Receptors, Interleukin-1 Type I/genetics ; Signal Transduction/genetics
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Grant Information:
K01 DK100616 United States DK NIDDK NIH HHS; R01 DK110586 United States DK NIDDK NIH HHS; R03 DK101817 United States DK NIDDK NIH HHS
Contributed Indexing:
Keywords: Immunology; Memory; Neuroscience; Obesity; Synapses
Substance Nomenclature:
0 (CX3C Chemokine Receptor 1)
0 (Cx3cr1 protein, mouse)
0 (IL1B protein, mouse)
0 (IL1R1 protein, mouse)
0 (Interleukin-1beta)
0 (NLR Family, Pyrin Domain-Containing 3 Protein)
0 (Nlrp3 protein, mouse)
0 (Receptors, Interleukin-1 Type I)
Entry Date(s):
Date Created: 20200115 Date Completed: 20201230 Latest Revision: 20201230
Update Code:
20240105
PubMed Central ID:
PMC7108893
DOI:
10.1172/JCI126078
PMID:
31935195
Czasopismo naukowe
Induction of the inflammasome protein cryopyrin (NLRP3) in visceral adipose tissue (VAT) promotes release of the proinflammatory cytokine IL-1β in obesity. Although this mechanism contributes to peripheral metabolic dysfunction, effects on the brain remain unexplored. We investigated whether visceral adipose NLRP3 impairs cognition by activating microglial IL-1 receptor 1 (IL-1R1). After observing protection against obesity-induced neuroinflammation and cognitive impairment in NLRP3-KO mice, we transplanted VAT from obese WT or NLRP3-KO donors into lean recipient mice. Transplantation of VAT from a WT donor (TRANSWT) increased hippocampal IL-1β and impaired cognition, but VAT transplants from comparably obese NLRP3-KO donors (TRANSKO) had no effect. Visceral adipose NLRP3 was required for deficits in long-term potentiation (LTP) in transplant recipients, and LTP impairment in TRANSWT mice was IL-1 dependent. Flow cytometric and gene expression analyses revealed that VAT transplantation recapitulated the effects of obesity on microglial activation and IL-1β gene expression, and visualization of hippocampal microglia revealed similar effects in vivo. Inducible ablation of IL-1R1 in CX3CR1-expressing cells eliminated cognitive impairment in mice with dietary obesity and in transplant recipients and restored immunoquiescence in hippocampal microglia. These results indicate that visceral adipose NLRP3 impairs memory via IL-1-mediated microglial activation and suggest that NLRP3/IL-1β signaling may underlie correlations between visceral adiposity and cognitive impairment in humans.

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