A Bartonella Effector Acts as Signaling Hub for Intrinsic STAT3 Activation to Trigger Anti-inflammatory Responses.
Amino Acid Sequence
Animals
Bacterial Proteins
/ metabolism
Bartonella henselae
/ immunology
Cell Line
Cytokines
/ immunology
Female
Interleukin-10
/ metabolism
Janus Kinases
/ metabolism
Mice
Mice, Inbred C57BL
Phosphorylation
RAW 264.7 Cells
STAT3 Transcription Factor
/ metabolism
Signal Transduction
Tumor Necrosis Factor-alpha
/ metabolism
Bartonella
BepD
EPIYA-related motif
STAT3
anti-inflammatory signaling
bacterial effector
c- Abl
chronic infection
interleukin 10
pro-inflammatory signaling
Journal
Cell host & microbe
ISSN: 1934-6069
Titre abrégé: Cell Host Microbe
Pays: United States
ID NLM: 101302316
Informations de publication
Date de publication:
11 03 2020
11 03 2020
Historique:
received:
21
10
2019
revised:
13
12
2019
accepted:
21
01
2020
pubmed:
27
2
2020
medline:
24
3
2020
entrez:
27
2
2020
Statut:
ppublish
Résumé
Chronically infecting pathogens avoid clearance by the innate immune system by promoting premature transition from an initial pro-inflammatory response toward an anti-inflammatory tissue-repair response. STAT3, a central regulator of inflammation, controls this transition and thus is targeted by numerous chronic pathogens. Here, we show that BepD, an effector of the chronic bacterial pathogen Bartonella henselae targeted to infected host cells, establishes an exceptional pathway for canonical STAT3 activation, thereby impairing secretion of pro-inflammatory TNF-α and stimulating secretion of anti-inflammatory IL-10. Tyrosine phosphorylation of EPIYA-related motifs in BepD facilitates STAT3 binding and activation via c-Abl-dependent phosphorylation of Y
Identifiants
pubmed: 32101706
pii: S1931-3128(20)30054-8
doi: 10.1016/j.chom.2020.01.015
pii:
doi:
Substances chimiques
Bacterial Proteins
0
Cytokines
0
IL10 protein, mouse
0
STAT3 Transcription Factor
0
Stat3 protein, mouse
0
Tumor Necrosis Factor-alpha
0
Interleukin-10
130068-27-8
Janus Kinases
EC 2.7.10.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
476-485.e7Subventions
Organisme : Swiss National Science Foundation
Pays : Switzerland
Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Interests The authors declare no competing interests.