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@ARTICLE{Wang:272488,
author = {Wang, Wei and Dernst, Alesja and Martin, Bianca and
Lorenzi, Lucia and Cadefau-Fabregat, Maria and Phulphagar,
Kshiti and Wagener, Antonia and Budden, Christina and Stair,
Neil and Wagner, Theresa and Färber, Harald and Jaensch,
Andreas and Stahl, Rainer and Duthie, Fraser and Schmidt,
Susanne V and Coll, Rebecca C and Meissner, Felix and
Cuartero, Sergi and Latz, Eicke and Mangan, Matthew},
title = {{B}utyrate and propionate are microbial danger signals that
activate the {NLRP}3 inflammasome in human macrophages upon
{TLR} stimulation.},
journal = {Cell reports},
volume = {43},
number = {9},
issn = {2211-1247},
address = {[New York, NY]},
publisher = {Elsevier},
reportid = {DZNE-2024-01169},
pages = {114736},
year = {2024},
abstract = {Short-chain fatty acids (SCFAs) are immunomodulatory
compounds produced by the microbiome through dietary fiber
fermentation. Although generally considered beneficial for
gut health, patients suffering from inflammatory bowel
disease (IBD) display poor tolerance to fiber-rich diets,
suggesting that SCFAs may have contrary effects under
inflammatory conditions. To investigate this, we examined
the effect of SCFAs on human macrophages in the presence of
Toll-like receptor (TLR) agonists. In contrast to
anti-inflammatory effects under steady-state conditions, we
found that butyrate and propionate activated the NOD-, LRR-,
and pyrin domain-containing protein 3 (NLRP3) inflammasome
in the presence of TLR agonists. Mechanistically, these
SCFAs prevented transcription of FLICE-like inhibitory
protein (cFLIP) and interleukin-10 (IL-10) through histone
deacetylase (HDAC) inhibition, triggering
caspase-8-dependent NLRP3 inflammasome activation.
SCFA-driven NLRP3 activation was potassium efflux
independent and did not result in cell death but rather
triggered hyperactivation and IL-1β release. Our findings
demonstrate that butyrate and propionate are bacterially
derived danger signals that regulate NLRP3 inflammasome
activation through epigenetic modulation of the inflammatory
response.},
keywords = {Humans / NLR Family, Pyrin Domain-Containing 3 Protein:
metabolism / Inflammasomes: metabolism / Propionates:
pharmacology / Butyrates: pharmacology / Macrophages:
metabolism / Macrophages: drug effects / Toll-Like
Receptors: metabolism / Signal Transduction: drug effects /
Interleukin-1beta: metabolism / Interleukin-10: metabolism /
CP: Immunology (Other) / HDAC (Other) / IL-10 (Other) /
NLRP3 (Other) / SCFA (Other) / acetylation (Other) /
butyrate (Other) / cFLIP (Other) / caspase-8 (Other) /
inflammasome (Other) / propionate (Other) / NLR Family,
Pyrin Domain-Containing 3 Protein (NLM Chemicals) /
Inflammasomes (NLM Chemicals) / Propionates (NLM Chemicals)
/ Butyrates (NLM Chemicals) / Toll-Like Receptors (NLM
Chemicals) / NLRP3 protein, human (NLM Chemicals) /
Interleukin-1beta (NLM Chemicals) / Interleukin-10 (NLM
Chemicals)},
cin = {AG Latz},
ddc = {610},
cid = {I:(DE-2719)1013024},
pnm = {351 - Brain Function (POF4-351)},
pid = {G:(DE-HGF)POF4-351},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39277863},
doi = {10.1016/j.celrep.2024.114736},
url = {https://pub.dzne.de/record/272488},
}