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STAT3 serine phosphorylation is required for TLR4 metabolic reprogramming and IL-1β expression.

Abstract：

:Detection of microbial components such as lipopolysaccharide (LPS) by Toll-like receptor 4 (TLR4) on macrophages induces a robust pro-inflammatory response that is dependent on metabolic reprogramming. These innate metabolic changes have been compared to aerobic glycolysis in tumour cells. However, the mechanisms by which TLR4 activation leads to mitochondrial and glycolytic reprogramming are unknown. Here we show that TLR4 activation induces a signalling cascade recruiting TRAF6 and TBK-1, while TBK-1 phosphorylates STAT3 on S727. Using a genetically engineered mouse model incapable of undergoing STAT3 Ser727 phosphorylation, we show ex vivo and in vivo that STAT3 Ser727 phosphorylation is critical for LPS-induced glycolytic reprogramming, production of the central immune response metabolite succinate and inflammatory cytokine production in a model of LPS-induced inflammation. Our study identifies non-canonical STAT3 activation as the crucial signalling intermediary for TLR4-induced glycolysis, macrophage metabolic reprogramming and inflammation.

journal_name

Nat Commun

journal_title

Nature communications

authors

Balic JJ,Albargy H,Luu K,Kirby FJ,Jayasekara WSN,Mansell F,Garama DJ,De Nardo D,Baschuk N,Louis C,Humphries F,Fitzgerald K,Latz E,Gough DJ,Mansell A

doi

10.1038/s41467-020-17669-5

subject

Has Abstract

pub_date

2020-07-30 00:00:00

pages

3816

issue

1

issn

2041-1723

pii

10.1038/s41467-020-17669-5

journal_volume

11

pub_type

杂志文章

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