AhR Activation Leads to Alterations in the Gut Microbiome with Consequent Effect on Induction of Myeloid Derived Suppressor Cells in a CXCR2-Dependent Manner.
Animals
Anti-Bacterial Agents
/ pharmacology
Basic Helix-Loop-Helix Transcription Factors
/ metabolism
Cells, Cultured
DNA, Bacterial
/ genetics
Dysbiosis
/ chemically induced
Fecal Microbiota Transplantation
/ methods
Feces
/ microbiology
Female
Gastrointestinal Microbiome
/ drug effects
Mice
Mice, Inbred C57BL
Myeloid-Derived Suppressor Cells
/ metabolism
Phylogeny
Polychlorinated Dibenzodioxins
/ adverse effects
Receptors, Aryl Hydrocarbon
/ metabolism
Receptors, Interleukin-8B
/ metabolism
Signal Transduction
/ drug effects
T-Lymphocytes, Regulatory
/ immunology
2,3,7,8-tetrachlorodibenzo-p-dioxin
CXCR2
aryl hydrocarbon receptor
microbiome
myeloid-derived suppressor cell
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
17 Dec 2020
17 Dec 2020
Historique:
received:
03
11
2020
revised:
27
11
2020
accepted:
12
12
2020
entrez:
22
12
2020
pubmed:
23
12
2020
medline:
16
3
2021
Statut:
epublish
Résumé
Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a potent ligand for AhR and a known carcinogen. While AhR activation by TCDD leads to significant immunosuppression, how this translates into carcinogenic signal is unclear. Recently, we demonstrated that activation of AhR by TCDD in naïve C57BL6 mice leads to massive induction of myeloid derived-suppressor cells (MDSCs). In the current study, we investigated the role of the gut microbiota in TCDD-mediated MDSC induction. TCDD caused significant alterations in the gut microbiome, such as increases in
Identifiants
pubmed: 33348596
pii: ijms21249613
doi: 10.3390/ijms21249613
pmc: PMC7767008
pii:
doi:
Substances chimiques
Ahr protein, mouse
0
Anti-Bacterial Agents
0
Basic Helix-Loop-Helix Transcription Factors
0
Cxcr2 protein, mouse
0
DNA, Bacterial
0
Polychlorinated Dibenzodioxins
0
Receptors, Aryl Hydrocarbon
0
Receptors, Interleukin-8B
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM103641
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI123947
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES030144
Pays : United States
Organisme : NIH HHS
ID : R01ES019313, R01MH094755, R01AI123947, R01AI129788, P01AT003961, P20GM103641, R01AT006888
Pays : United States
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