SCFAs promote intestinal double-negative T cells to regulate the inflammatory response mediated by NLRP3 inflammasome.
Alzheimer Disease
/ metabolism
Animals
Brain
/ metabolism
Cytokines
/ metabolism
Disease Models, Animal
Fas Ligand Protein
/ metabolism
Fatty Acids, Volatile
/ metabolism
Inflammasomes
/ metabolism
Inflammation
Intestines
/ immunology
Macrophages
/ metabolism
Mice, Inbred C57BL
Mice, Transgenic
NLR Family, Pyrin Domain-Containing 3 Protein
/ metabolism
Neuroinflammatory Diseases
/ metabolism
Receptors, OX40
/ metabolism
T-Lymphocytes
/ metabolism
Tumor Necrosis Factor-alpha
/ metabolism
fas Receptor
/ metabolism
Alzheimer’s disease
NLRP3
double-negative T cells
neuroinflammation
short-chain fatty acids
Journal
Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617
Informations de publication
Date de publication:
07 09 2021
07 09 2021
Historique:
received:
01
07
2021
accepted:
11
08
2021
pubmed:
8
9
2021
medline:
4
1
2022
entrez:
7
9
2021
Statut:
ppublish
Résumé
Short-chain fatty acids (SCFAs) are a product of intestinal bacteria metabolism. Our previous study has found that intestinal bacteria in patients with Alzheimer's disease (AD) can promote the activation of NLRP3 inflammasome and mediate neuroinflammation. In this study, we mainly explored the regulation of intestinal microenvironmental immunity by intestinal bacterial metabolite SCFAs and the mechanism of NLRP3 activation. First, wild-type (WT) and APP/PS1 mice were intervened with SCFAs. As a result, the proportion of double-negative T cells (CD3
Identifiants
pubmed: 34491906
pii: 203487
doi: 10.18632/aging.203487
pmc: PMC8457588
doi:
Substances chimiques
Cytokines
0
Fas Ligand Protein
0
Fas protein, mouse
0
Fasl protein, mouse
0
Fatty Acids, Volatile
0
Inflammasomes
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Nlrp3 protein, mouse
0
Receptors, OX40
0
Tnf protein, mouse
0
Tnfrsf4 protein, mouse
0
Tumor Necrosis Factor-alpha
0
fas Receptor
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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