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BPTES inhibits anthrax lethal toxin-induced inflammatory response.

Abstract：

:Bacillus anthracis is a lethal agent of anthrax disease and the toxins are required in anthrax pathogenesis. The anthrax lethal toxin can trigger NLRP1b inflammasome activation and pyroptosis. Although the underlying mechanism is well understood, the medications targeting the NLRP1b inflammasome are not available in the clinic. Herein, we describe that BPTES, a known Glutaminase (GLS) inhibitor, is an effective NLRP1b inflammasome inhibitor. BPTES could effectively and specifically suppress NLRP1b inflammasome activation in macrophages but have no effects on NLRP3, NLRC4 and AIM2 inflammasome activation. Mechanistically, BPTES alleviated the UBR2 mediated proteasomal degradation pathway of the NLRP1b N terminus, thus blocking the release of the CARD domain for subsequent caspase-1 processing. Furthermore, BPTES could prevent disease progression in mice challenged with the anthrax lethal toxin. Taken together, our studies indicate that BPTES can be a promising pharmacological inhibitor to treat anthrax lethal toxin-related inflammatory diseases.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Wang J,Yang D,Shen X,Wang J,Liu X,Lin J,Zhong J,Zhao Y,Qi Z

doi

10.1016/j.intimp.2020.106664

subject

Has Abstract

pub_date

2020-08-01 00:00:00

pages

106664

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(20)31379-5

journal_volume

85

pub_type

杂志文章

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