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@ARTICLE{Gttert:163462,
author = {Göttert, Ria and Fidzinski, Pawel and Kraus, Larissa and
Schneider, Ulf Christoph and Holtkamp, Martin and Endres,
Matthias and Gertz, Karen and Kronenberg, Golo},
title = {{L}ithium inhibits tryptophan catabolism via the
inflammation-induced kynurenine pathway in human microglia.},
journal = {Glia},
volume = {70},
number = {3},
issn = {1098-1136},
address = {Bognor Regis [u.a.]},
publisher = {Wiley-Liss},
reportid = {DZNE-2022-00222},
pages = {558 - 571},
year = {2022},
note = {(CC BY-NC)},
abstract = {Despite its decades' long therapeutic use in psychiatry,
the biological mechanisms underlying lithium's
mood-stabilizing effects have remained largely elusive.
Here, we investigated the effect of lithium on tryptophan
breakdown via the kynurenine pathway using immortalized
human microglia cells, primary human microglia isolated from
surgical specimens, and microglia-like cells differentiated
from human induced pluripotent stem cells. Interferon
(IFN)-γ, but not lipopolysaccharide, was able to activate
immortalized human microglia, inducing a robust increase in
indoleamine-2,3-dioxygenase (IDO1) mRNA transcription, IDO1
protein expression, and activity. Further, chromatin
immunoprecipitation verified enriched binding of both STAT1
and STAT3 to the IDO1 promoter. Lithium counteracted these
effects, increasing inhibitory GSK3βS9 phosphorylation and
reducing STAT1S727 and STAT3Y705 phosphorylation levels in
IFN-γ treated cells. Studies in primary human microglia and
hiPSC-derived microglia confirmed the anti-inflammatory
effects of lithium, highlighting that IDO activity is
reduced by GSK3 inhibitor SB-216763 and STAT inhibitor
nifuroxazide via downregulation of P-STAT1S727 and
P-STAT3Y705 . Primary human microglia differed from
immortalized human microglia and hiPSC derived
microglia-like cells in their strong sensitivity to LPS,
resulting in robust upregulation of IDO1 and
anti-inflammatory cytokine IL-10. While lithium again
decreased IDO1 activity in primary cells, it further
increased release of IL-10 in response to LPS. Taken
together, our study demonstrates that lithium inhibits the
inflammatory kynurenine pathway in the microglia compartment
of the human brain.},
keywords = {Glycogen Synthase Kinase 3: metabolism / Glycogen Synthase
Kinase 3: pharmacology / Humans / Indoleamine-Pyrrole
2,3,-Dioxygenase: genetics / Indoleamine-Pyrrole
2,3,-Dioxygenase: metabolism / Indoleamine-Pyrrole
2,3,-Dioxygenase: pharmacology / Induced Pluripotent Stem
Cells: metabolism / Inflammation: metabolism / Kynurenine:
metabolism / Kynurenine: pharmacology / Lithium: metabolism
/ Lithium: pharmacology / Microglia: metabolism /
Tryptophan: metabolism / Tryptophan: pharmacology /
depression (Other) / kynurenine (Other) / lithium (Other) /
microglia (Other) / tryptophan (Other) / Indoleamine-Pyrrole
2,3,-Dioxygenase (NLM Chemicals) / Kynurenine (NLM
Chemicals) / Tryptophan (NLM Chemicals) / Lithium (NLM
Chemicals) / Glycogen Synthase Kinase 3 (NLM Chemicals)},
cin = {AG Endres},
ddc = {610},
cid = {I:(DE-2719)1811005},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34862988},
doi = {10.1002/glia.24123},
url = {https://pub.dzne.de/record/163462},
}