Polydatin通过抑制Caspase1/GSDMD依赖性pyroptosis减轻肺炎支原体诱导的损伤。

IF 4.5 3区 医学 Q1 MICROBIOLOGY International Journal of Medical Microbiology Pub Date : 2023-09-01 DOI:10.1016/j.ijmm.2023.151586
Yiliu Chen , Yonghong Jiang , Xiuxiu Liu, Xiufeng Chen, Qiuyue Fan, Zhen Xiao
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引用次数: 0

摘要

肺炎支原体(MP)是引起儿童和成人社区获得性肺炎(CAP)的主要病原体之一。先前的药理学和临床研究表明,Polydatin(PD)通过对MP肺炎的保护作用发挥抗炎作用。然而,帕金森病对MP感染的潜在机制尚不清楚。研究发现,PD通过抑制胱天蛋白酶1/gasdermin D(GSDMD)介导的上皮焦下垂来减轻MP诱导的损伤。结果表明,PD通过降低胱天蛋白酶-1的激活来抑制GSDMD向N-末端gasdermin-N(GSDMD-N)的转化,并在体内外抑制白细胞介素-1β(IL-1β)和IL-18的形成和分泌,逆转Na、K-ATP酶的减少,抑制LDH的释放。总之,PD可以预防BEAS-2B细胞的上皮性pyroptosis和小鼠的肺损伤。总之,PD通过抑制胱天蛋白酶1/GSDMD介导的上皮性pyroptosis信号通路来抑制MP感染引发的肺损伤。因此,PD可被视为MP诱导炎症的潜在治疗方法。
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Polydatin alleviates mycoplasma pneumoniae-induced injury via inhibition of Caspase-1/GSDMD-dependent pyroptosis

Mycoplasma pneumoniae (MP) is one of the main pathogens causing community acquired pneumonia (CAP) in children and adults. Previous pharmacological and clinical studies have shown that Polydatin (PD) exerts anti-inflammatory action by conferring protective benefit in MP pneumonia. However, the mechanism underlying the of PD on MP infection remains unclear. It was found that PD alleviated MP-induced injury by inhibiting caspase-1/gasdermin D (GSDMD)-mediated epithelial pyroptosis. The results demonstrated that PD inhibited the transformation of GSDMD to N-terminal gasdermin-N (GSDMD-N) by decreasing caspase-1 activation, as well as suppressed the formation and secretion of interleukin-1β (IL-1β) and interleukin-18 (IL-18), reversed Na, K-ATPase reduction, and suppressed LDH release both in vitro and vivo. Taken together, epithelial pyroptosis in BEAS‐2B cells and lung injury in mice were prevented by PD. In conclusion, PD suppressed pulmonary injury triggered by MP infection, by inhibiting the caspase-1/GSDMD-mediated epithelial pyroptosis signaling pathway. Thus, PD may be regarded as a potential therapy for MP-induced inflammation.

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来源期刊
CiteScore
9.70
自引率
0.00%
发文量
18
审稿时长
45 days
期刊介绍: Pathogen genome sequencing projects have provided a wealth of data that need to be set in context to pathogenicity and the outcome of infections. In addition, the interplay between a pathogen and its host cell has become increasingly important to understand and interfere with diseases caused by microbial pathogens. IJMM meets these needs by focussing on genome and proteome analyses, studies dealing with the molecular mechanisms of pathogenicity and the evolution of pathogenic agents, the interactions between pathogens and host cells ("cellular microbiology"), and molecular epidemiology. To help the reader keeping up with the rapidly evolving new findings in the field of medical microbiology, IJMM publishes original articles, case studies and topical, state-of-the-art mini-reviews in a well balanced fashion. All articles are strictly peer-reviewed. Important topics are reinforced by 2 special issues per year dedicated to a particular theme. Finally, at irregular intervals, current opinions on recent or future developments in medical microbiology are presented in an editorial section.
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