Leptin signaling impairs macrophage defenses against
Adult
Animals
Female
Humans
Inflammation
/ pathology
Leptin
/ antagonists & inhibitors
Lysosomes
/ metabolism
Macrophages
/ immunology
Mechanistic Target of Rapamycin Complex 2
/ metabolism
Mice
Mice, Inbred C57BL
Models, Biological
Phagosomes
/ metabolism
Phosphoprotein Phosphatases
/ metabolism
Phosphorylation
Proto-Oncogene Proteins c-akt
/ metabolism
RAW 264.7 Cells
Receptors, Leptin
/ metabolism
Salmonella Infections, Animal
Salmonella typhimurium
/ immunology
Signal Transduction
Young Adult
AKT
Salmonella
leptin
lysosomes
macrophages
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
13 08 2019
13 08 2019
Historique:
pubmed:
28
7
2019
medline:
26
3
2020
entrez:
28
7
2019
Statut:
ppublish
Résumé
The dynamic interplay between metabolism and immune responses in health and disease, by which different immune cells impact on metabolic processes, are being increasingly appreciated. However, the potential of master regulators of metabolism to control innate immunity are less understood. Here, we studied the cross-talk between leptin signaling and macrophage function in the context of bacterial infections. We found that upon infection with Gram-negative pathogens, such as
Identifiants
pubmed: 31350351
pii: 1904885116
doi: 10.1073/pnas.1904885116
pmc: PMC6697794
doi:
Substances chimiques
Leptin
0
Receptors, Leptin
0
Mechanistic Target of Rapamycin Complex 2
EC 2.7.11.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
PHLPP1 protein, mouse
EC 3.1.3.16
Phosphoprotein Phosphatases
EC 3.1.3.16
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
16551-16560Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK026687
Pays : United States
Informations de copyright
Copyright © 2019 the Author(s). Published by PNAS.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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