血清型5副猪小绿杆菌通过降解Caveolin-1促进3D4/21细胞的焦亡。

IF 2.4 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology Pub Date : 2025-01-13 DOI:10.1016/j.vetmic.2025.110393

Huixing Lin , Jianan Zhang , Qing Wang , Hong Zhou , Hongjie Fan

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引用次数: 0

摘要

副猪Glaesserella parasuis （G. parasuis）是一种重要的病原体，可引起猪的全身炎症反应，给全球养猪业带来巨大的经济损失。副猪绦虫在环境变化和一定应激条件下可引起肺部强烈的炎症反应。然而，这种不良反应的潜在机制尚未得到充分研究。在本研究中，我们证实了副猪螺旋体血清5型菌株（GPS5-SQ）在3D4/21细胞中具有诱导焦亡的潜力。GPS5-SQ可降低Cav-1的表达。敲低或过表达Cav-1分别促进或减少焦亡的发生。提示Cav-1参与了GPS5-SQ诱导3D4/21细胞的焦亡。此外，过表达Cav-1通过抑制ASC寡聚化抑制NLRP3炎性体的激活，导致焦亡减少。总的来说，我们发现GPS5-SQ感染可以通过降低Cav-1的表达来促进焦亡。本研究结果揭示了GPS5-SQ诱导3D4/21细胞炎症的新机制。

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Glaesserella parasuis serotype 5 promotes pyroptosis via degrading Caveolin-1 in 3D4/21 cells

Glaesserella parasuis (G. parasuis) is an important pathogen, which can cause systemic inflammatory response in pigs and bring huge economic losses to the global swine industry. G. parasuis can induce a strong inflammatory response in the lungs under environmental changes and certain stress conditions. However, the underlying mechanism of this adverse response has not been thoroughly studied. In this study we demonstrated that G. parasuis serotype 5 strain (GPS5-SQ) has the potential to induce pyroptosis in 3D4/21 cells. GPS5-SQ could degrade the expression of Cav-1. Knockdown or overexpression of Cav-1 promoted or reduced the occurrence of pyroptosis, respectively. These results suggested that Cav-1 is involved in pyroptosis induced by GPS5-SQ in 3D4/21 cells. In addition, overexpression of Cav-1 suppressed the activation of NLRP3 inflammasome by inhibiting ASC oligomerization, resulted in reducing pyroptosis. In general, we found that GPS5-SQ infection could promote pyroptosis by degrading the expression of Cav-1. The results of the study revealed the new mechanism of inflammation induced by GPS5-SQ in 3D4/21 cells.

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来源期刊

Veterinary microbiology 农林科学-兽医学

CiteScore

5.90

自引率

6.10%

发文量

221

审稿时长

52 days

期刊介绍： Veterinary Microbiology is concerned with microbial (bacterial, fungal, viral) diseases of domesticated vertebrate animals (livestock, companion animals, fur-bearing animals, game, poultry, fish) that supply food, other useful products or companionship. In addition, Microbial diseases of wild animals living in captivity, or as members of the feral fauna will also be considered if the infections are of interest because of their interrelation with humans (zoonoses) and/or domestic animals. Studies of antimicrobial resistance are also included, provided that the results represent a substantial advance in knowledge. Authors are strongly encouraged to read - prior to submission - the Editorials (''Scope or cope'' and ''Scope or cope II'') published previously in the journal. The Editors reserve the right to suggest submission to another journal for those papers which they feel would be more appropriate for consideration by that journal. Original research papers of high quality and novelty on aspects of control, host response, molecular biology, pathogenesis, prevention, and treatment of microbial diseases of animals are published. Papers dealing primarily with immunology, epidemiology, molecular biology and antiviral or microbial agents will only be considered if they demonstrate a clear impact on a disease. Papers focusing solely on diagnostic techniques (such as another PCR protocol or ELISA) will not be published - focus should be on a microorganism and not on a particular technique. Papers only reporting microbial sequences, transcriptomics data, or proteomics data will not be considered unless the results represent a substantial advance in knowledge. Drug trial papers will be considered if they have general application or significance. Papers on the identification of microorganisms will also be considered, but detailed taxonomic studies do not fall within the scope of the journal. Case reports will not be published, unless they have general application or contain novel aspects. Papers of geographically limited interest, which repeat what had been established elsewhere will not be considered. The readership of the journal is global.