Virulence最新文献

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Serine protease RAYM_01812 (SspA) inhibits complement-mediated killing and monocyte chemotaxis and contributes to virulence of Riemerella anatipestifer in ducks. 丝氨酸蛋白酶 RAYM_01812 (SspA) 可抑制补体介导的杀伤作用和单核细胞趋化作用,并有助于提高鸭毒酵母菌的毒力。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-11-04 DOI: 10.1080/21505594.2024.2421219
Rongkun Yang, Sen Li, Jie Guo, Yanhua Wang, Zeyuan Dong, Qing Wang, Hongying Bai, Congran Ning, Xiaotong Zhu, Jiao Bai, Sishun Hu, Yuncai Xiao, Zili Li, Zutao Zhou
{"title":"Serine protease RAYM_01812 (SspA) inhibits complement-mediated killing and monocyte chemotaxis and contributes to virulence of <i>Riemerella anatipestifer</i> in ducks.","authors":"Rongkun Yang, Sen Li, Jie Guo, Yanhua Wang, Zeyuan Dong, Qing Wang, Hongying Bai, Congran Ning, Xiaotong Zhu, Jiao Bai, Sishun Hu, Yuncai Xiao, Zili Li, Zutao Zhou","doi":"10.1080/21505594.2024.2421219","DOIUrl":"10.1080/21505594.2024.2421219","url":null,"abstract":"<p><p><i>Riemerella anatipestifer</i> (RA) is a significant poultry pathogen causing acute septicemia and inflammation. The function of protease RAYM_01812, responsible for gelatin degradation, is unexplored in RA pathogenesis. To elucidate its role, we generated a deletion mutant ΔRAYM_01812 (ΔRAYM) and complementary CΔRAYM_01812 (CΔRAYM) strain and revealed the protease's role in extracellular gelatinase activity. By expressing full-length 76 kDa RAYM_01812 protein without signal peptide as well as seven partial structural domains fragments, we evidence that the N-terminal propeptide acts as an enzymatic activity inhibitor and it gets cleaved at A<sup>112</sup>. Also, we show that the β-fold sheet domain is necessary for enhancing the enzymatic protease activity. Sequential auto-proteolysis forms a stable 40 kDa enzyme. Then, testing the strains in duck sera indicated that the absence or presence of RAYM_01812 results in reduced or enhanced bacterial survival, respectively. Furthermore, we found that the protease is able to cleave IgY antibodies as well as the complement factors C3a and C5a, that the protease reduces C3a- or C5a-mediated monocyte chemotaxis, and results in enhanced membrane attack complex (MAC) formation on the surface of ΔRAYM compared to CΔRAYM. This suggests that RAYM_01812 plays a crucial role in protecting against the serum complement-mediated bactericidal effect through inhibiting MAC formation and monocyte chemotaxis. Animal infection assays showed a 1090-fold reduced virulence of ΔRAYM compared to RA-YM, evidenced by decreased tissue loading and weaker histopathological changes. In conclusion, RAYM_01812 acts as a vital virulence factor, enabling host innate immune defence escape through complement killing evasion and monocyte chemotaxis inhibition.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142509210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The arginine/ornithine binding protein ArgT plays an essential role in Brucella neotomae/Brucella melitensis to prevent intracellular killing and contribute to chronic persistence in the host. 精氨酸/鸟氨酸结合蛋白 ArgT 在新布鲁氏菌/梅毒布鲁氏菌中发挥着重要作用,可防止细胞内杀灭,并有助于在宿主体内长期存活。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-11-04 DOI: 10.1080/21505594.2024.2421983
Sushree Rekha Mallik, Kiranmai Joshi, Girish K Radhakrishnan
{"title":"The arginine/ornithine binding protein ArgT plays an essential role in <i>Brucella neotomae</i>/<i>Brucella melitensis</i> to prevent intracellular killing and contribute to chronic persistence in the host.","authors":"Sushree Rekha Mallik, Kiranmai Joshi, Girish K Radhakrishnan","doi":"10.1080/21505594.2024.2421983","DOIUrl":"10.1080/21505594.2024.2421983","url":null,"abstract":"<p><p><i>Brucella</i> species are facultative intracellular bacterial pathogens that cause the contagious zoonotic disease, brucellosis. <i>Brucella</i> spp. infect a wide range of animals, including livestock, wild animals, and marine mammals. Compared with other invasive bacterial pathogens, partial information is available on the virulence factors of <i>Brucella</i> that enable them to survive in the host. Here, we performed transposon-based random mutagenesis of <i>B. neotomae</i> and identified the arginine/ornithine binding protein, ArgT, as one of the crucial virulence determinants of <i>Brucella</i>. Deleting <i>ArgT</i> from <i>B. neotomae</i> or <i>B. melitensis</i> resulted in its attenuation in macrophages, which was restored upon complementation with an <i>ArgT</i> expression plasmid. We observed that macrophages infected with Δ<i>ArgT-B. neotomae</i> produced elevated levels of NO due to the inability of these mutants to deplete the host intracellular arginine through their importer. Furthermore, defective survival of Δ<i>ArgT B. neotomae</i> and <i>B. melitensis</i> was observed in the infected mice, which correlated with enhanced NO production in the mice. Our studies revealed that <i>ArgT</i> plays a vital role in preventing intracellular killing and contributes to the chronic persistence of <i>B. neotomae/B. melitensis</i> in the host. This study highlights the essential role of arginine in clearing intracellular infections and the subversion of this host defense mechanism by intracellular pathogens for their chronic persistence.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142509225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Deletion of glycosyltransferase galE impairs the InlB anchoring and pathogenicity of Listeria monocytogenes. 糖基转移酶 galE 的缺失会损害单核细胞增多性李斯特菌的 InlB 锚定和致病性。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-11-04 DOI: 10.1080/21505594.2024.2422539
Xiaowei Fang, Mei Yuan, Minghao Zheng, Qian Guo, Yuting Yang, Yuying Yang, Xiongyan Liang, Jing Liu, Chun Fang
{"title":"Deletion of glycosyltransferase <i>galE</i> impairs the InlB anchoring and pathogenicity of <i>Listeria monocytogenes</i>.","authors":"Xiaowei Fang, Mei Yuan, Minghao Zheng, Qian Guo, Yuting Yang, Yuying Yang, Xiongyan Liang, Jing Liu, Chun Fang","doi":"10.1080/21505594.2024.2422539","DOIUrl":"10.1080/21505594.2024.2422539","url":null,"abstract":"<p><p><i>Listeria monocytogenes</i> (<i>L. monocytogenes</i>) is a foodborne intracellular pathogen that causes serious disease in both humans and animals. InlB is the major internalin protein of <i>L. monocytogenes</i>, which anchors to the bacterial surface and mediates its invasion into various host cells. Recent studies have shown that galactosylation of the cell wall polymer wall teichoic acid (WTA) is essential for InlB anchoring on the cell surface of <i>L. monocytogenes</i> serotype 4b strains. Galactosylation of WTA is exerted by the coordinated action of several glycosyltransferases, including GalU, GalE, GtcA, GttA, and GttB. Among these glycosyltransferases, GttA and GttB are specific to serotype 4b strains, whereas GalE, GalU, and GtcA are conserved across all serotypes. The role of GalE in InlB anchoring and <i>L. monocytogenes</i> pathogenicity remains unclear. In this study, we deleted the <i>galE</i> gene, which is involved in galactosylation, from <i>L. monocytogenes</i> strain ScottA. We found that <i>galE</i> deletion reduced InlB anchoring, weakened bacterial adhesion and invasion of Caco-2 cells (human colorectal adenocarcinoma cells) and MGC803 cells (human gastric carcinoma cells), increased phagocytosis but decreased proliferation in RAW264.7 cells (mouse mononuclear macrophage leukaemia cells), and decreased bacteria load, mortality, and tissue damage in infected mice. Taken together, <i>galE</i> deletion significantly reduced the anchoring of InlB and weakened the pathogenicity of <i>L. monocytogenes</i>. This finding provides new insights into the correlation between cell wall modification and pathogenicity of <i>L. monocytogenes</i>.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The intricate pathogenicity of Group A Streptococcus: A comprehensive update. a 群链球菌的复杂致病性:全面更新。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-11-05 DOI: 10.1080/21505594.2024.2412745
Helena Bergsten, Victor Nizet
{"title":"The intricate pathogenicity of Group A <i>Streptococcus</i>: A comprehensive update.","authors":"Helena Bergsten, Victor Nizet","doi":"10.1080/21505594.2024.2412745","DOIUrl":"10.1080/21505594.2024.2412745","url":null,"abstract":"<p><p>Group A <i>Streptococcus</i> (GAS) is a versatile pathogen that targets human lymphoid, decidual, skin, and soft tissues. Recent advancements have shed light on its airborne transmission, lymphatic spread, and interactions with neuronal systems. GAS promotes severe inflammation through mechanisms involving inflammasomes, IL-1β, and T-cell hyperactivation. Additionally, it secretes factors that directly induce skin necrosis via Gasdermin activation and sustains survival and replication in human blood through sophisticated immune evasion strategies. These include lysis of erythrocytes, using red cell membranes for camouflage, resisting antimicrobial peptides, evading phagocytosis, escaping from neutrophil extracellular traps (NETs), inactivating chemokines, and cleaving targeted antibodies. GAS also employs molecular mimicry to traverse connective tissues undetected and exploits the host's fibrinolytic system, which contributes to its stealth and potential for causing autoimmune conditions after repeated infections. Secreted toxins disrupt host cell membranes, enhancing intracellular survival and directly activating nociceptor neurons to induce pain. Remarkably, GAS possesses mechanisms for precise genome editing to defend against phages, and its fibrinolytic capabilities have found applications in medicine. Immune responses to GAS are paradoxical: robust responses to its virulence factors correlate with more severe disease, whereas recurrent infections often show diminished immune reactions. This review focuses on the multifaceted virulence of GAS and introduces novel concepts in understanding its pathogenicity.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11542602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Functional characterization of BbEaf6 in Beauveria bassiana: Implications for fungal virulence and stress response. BbEaf6 的功能表征,BbEaf6 是 Beauveria bassiana 中 Eaf6 的同源物:对真菌毒力和应激反应的影响。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-08-01 DOI: 10.1080/21505594.2024.2387172
Qing Cai, Juan-Juan Wang, Jia-Tao Xie, Dao-Hong Jiang
{"title":"Functional characterization of BbEaf6 in <i>Beauveria bassiana</i>: Implications for fungal virulence and stress response.","authors":"Qing Cai, Juan-Juan Wang, Jia-Tao Xie, Dao-Hong Jiang","doi":"10.1080/21505594.2024.2387172","DOIUrl":"10.1080/21505594.2024.2387172","url":null,"abstract":"<p><p>The Eaf6 protein, a conserved component of the NuA4 and NuA3 complexes in yeast and MOZ/MORF complexes in humans, plays crucial roles in transcriptional activation, gene regulation, and cell cycle control. Despite its significance in other organisms, the functional role of Eaf6 in entomopathogenic fungi (EPF) remained unexplored. Here, we investigate the function of BbEaf6, the Eaf6 homolog in the entomopathogenic fungus <i>Beauveria bassiana</i>. We demonstrate that BbEaf6 is predominantly localized in nuclei, similar to its counterpart in other fungi. Deletion of <i>BbEaf6</i> resulted in delayed conidiation, reduced conidial yield, and altered conidial properties. Transcriptomic analysis revealed dysregulation of the genes involved in asexual development and cell cycle progression in the Δ<i>BbEaf6</i> mutant. Furthermore, the Δ<i>BbEaf6</i> mutant exhibited decreased tolerance to various stresses, including ionic stress, cell wall perturbation, and DNA damage stress. Notably, the Δ<i>BbEaf6</i> mutant displayed attenuated virulence in insect bioassays, accompanied by dysregulation of genes associated with cuticle penetration and haemocoel infection. Overall, our study elucidates the multifaceted role of BbEaf6 in stress response, development, and virulence in <i>B. bassiana</i>, providing valuable insights into the molecular mechanisms governing fungal pathogenesis and potential targets for pest management strategies.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11299629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141856636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dengue fever in the Americas. 美洲登革热。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-07-11 DOI: 10.1080/21505594.2024.2375551
Hinh Ly
{"title":"Dengue fever in the Americas.","authors":"Hinh Ly","doi":"10.1080/21505594.2024.2375551","DOIUrl":"10.1080/21505594.2024.2375551","url":null,"abstract":"","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11244333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141580988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
In silico identification of novel pre-microRNA genes in Rift valley fever virus suggest new pathomechanisms for embryo-fetal dysgenesis. 裂谷热病毒中新型前微小核糖核酸基因的硅学鉴定提示了胚胎-胎儿发育不良的新病理机制。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-03-28 DOI: 10.1080/21505594.2024.2329447
Balal Sadeghi, Martin H Groschup, Martin Eiden
{"title":"In silico identification of novel pre-microRNA genes in Rift valley fever virus suggest new pathomechanisms for embryo-fetal dysgenesis.","authors":"Balal Sadeghi, Martin H Groschup, Martin Eiden","doi":"10.1080/21505594.2024.2329447","DOIUrl":"10.1080/21505594.2024.2329447","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) are small non-coding RNAs that regulate the post-transcriptional expression of target genes. Virus-encoded miRNAs play an important role in the replication of viruses, modulate gene expression in both the virus and host, and affect their persistence and immune evasion in hosts. This renders viral miRNAs as potential targets for therapeutic applications, especially against pathogenic viruses that infect humans and animals. Rift Valley fever virus (RVFV) is a mosquito-borne zoonotic RNA virus that causes severe disease in both humans and livestock. High mortality among newborn lambs and abortion storms are key characteristics of an RVF outbreak. To date, limited information is available on RVFV-derived miRNAs. In this study, computational methods were used to analyse the RVFV genome for putative pre-miRNA genes, which were then analysed for the presence of mature miRNAs. We detected 19 RVFV-encoded miRNAs and identified their potential mRNAs targets in sheep (<i>Ovis aries)</i>, the most susceptible host. The identification of significantly enriched <i>O. aries</i> genes in association with RVFV miRNAs will help elucidate the molecular mechanisms underlying RVFV pathogenesis and potentially uncover novel drug targets for RVFV.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10984114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140319395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Role of cell membrane homeostasis in the pathogenicity of pathogenic filamentous fungi. 细胞膜稳态在致病性丝状真菌致病性中的作用。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2023-12-29 DOI: 10.1080/21505594.2023.2299183
Yuejin Peng, Bin Chen
{"title":"Role of cell membrane homeostasis in the pathogenicity of pathogenic filamentous fungi.","authors":"Yuejin Peng, Bin Chen","doi":"10.1080/21505594.2023.2299183","DOIUrl":"10.1080/21505594.2023.2299183","url":null,"abstract":"<p><p>The cell membrane forms a fundamental part of all living cells and participates in a variety of physiological processes, such as material exchange, stress response, cell recognition, signal transduction, cellular immunity, apoptosis, and pathogenicity. Here, we review the mechanisms and functions of the membrane structure (lipid components of the membrane and the biosynthesis of unsaturated fatty acids), membrane proteins (transmembrane proteins and proteins contributing to membrane curvature), transcriptional regulation, and cell wall components that influence the virulence and pathogenicity of filamentous fungi.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10761126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139075208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Genomic island-encoded regulatory proteins in enterohemorrhagic Escherichia coli O157:H7. 肠出血性大肠杆菌 O157:H7 的基因组岛编码调控蛋白。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-02-15 DOI: 10.1080/21505594.2024.2313407
Fang Wang, Hongmin Sun, Chenbo Kang, Jun Yan, Jingnan Chen, Xuequan Feng, Bin Yang
{"title":"Genomic island-encoded regulatory proteins in enterohemorrhagic <i>Escherichia coli</i> O157:H7.","authors":"Fang Wang, Hongmin Sun, Chenbo Kang, Jun Yan, Jingnan Chen, Xuequan Feng, Bin Yang","doi":"10.1080/21505594.2024.2313407","DOIUrl":"10.1080/21505594.2024.2313407","url":null,"abstract":"<p><p>Enterohemorrhagic <i>Escherichia coli</i> (EHEC) is an important zoonotic pathogen that is a major cause of foodborne diseases in most developed and developing countries and can cause uncomplicated diarrhoea, haemorrhagic colitis, and haemolytic uraemic syndrome. O islands (OIs), which are unique genomic islands in EHEC O157:H7, are composed of 177 isolated genomic features and harbour 26% of the total genes that are absent in the non-pathogenic <i>E. coli</i> K-12 genome. In the last twenty years, many OI-encoded proteins have been characterized, including proteins regulating virulence, motility, and acid resistance. Given the critical role of regulatory proteins in the systematic and hierarchical regulation of bacterial biological processes, this review summarizes the OI-encoded regulatory proteins in EHEC O157:H7 characterized to date, emphasizing OI-encoded regulatory proteins for bacterial virulence, motility, and acid resistance. This summary will be significant for further exploration and understanding of the virulence and pathogenesis of EHEC O157:H7.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10877973/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139736236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Staphylococcus pseudintermedius induces pyroptosis of canine corneal epithelial cells by activating the ROS-NLRP3 signalling pathway. 假中间葡萄球菌通过激活 ROS-NLRP3 信号通路诱导犬角膜上皮细胞发生热昏迷。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-03-31 DOI: 10.1080/21505594.2024.2333271
Zhihao Wang, Long Guo, Changning Yuan, Chengcheng Zhu, Jun Li, Haoran Zhong, Peng Mao, Jianji Li, Luying Cui, Junsheng Dong, Kangjun Liu, Xia Meng, Guoqiang Zhu, Heng Wang
{"title":"Staphylococcus pseudintermedius induces pyroptosis of canine corneal epithelial cells by activating the ROS-NLRP3 signalling pathway.","authors":"Zhihao Wang, Long Guo, Changning Yuan, Chengcheng Zhu, Jun Li, Haoran Zhong, Peng Mao, Jianji Li, Luying Cui, Junsheng Dong, Kangjun Liu, Xia Meng, Guoqiang Zhu, Heng Wang","doi":"10.1080/21505594.2024.2333271","DOIUrl":"10.1080/21505594.2024.2333271","url":null,"abstract":"<p><p><i>Staphylococcus pseudintermedius</i> (<i>S. pseudintermedius</i>) is a common pathogen that causes canine corneal ulcers. However, the pathogenesis remained unclear. In this study, it has been demonstrated that <i>S. pseudintermedius</i> invaded canine corneal epithelial cells (CCECs) intracellularly, mediating oxidative damage and pyroptosis by promoting the accumulation of intracellular reactive oxygen species (ROS) and activating the NLRP3 inflammasome. The canine corneal stroma was infected with <i>S. pseudintermedius</i> to establish the canine corneal ulcer model in vivo. The intracellular infectious model in CCECs was established in vitro to explore the mechanism of the ROS - NLRP3 signalling pathway during the <i>S. pseudintermedius</i> infection by adding NAC or MCC950. Results showed that the expression of NLRP3 and gasdermin D (GSDMD) proteins increased significantly in the infected corneas (<i>p <</i> 0.01). The intracellular infection of <i>S. pseudintermedius</i> was confirmed by transmission electron microscopy and immunofluorescent 3D imaging. Flow cytometry analysis revealed that ROS and pyroptosis rates increased in the experimental group in contrast to the control group (<i>p</i> < 0.01). Furthermore, NAC or MCC950 inhibited activation of the ROS - NLRP3 signalling pathway and pyroptosis rate significantly, by suppressing pro-IL-1β, cleaved-IL-1β, pro-caspase-1, cleaved-caspase-1, NLRP3, GSDMD, GSDMD-N, and HMGB1 proteins. Thus, the research confirmed that oxidative damage and pyroptosis were involved in the process of CCECs infected with <i>S. pseudintermedius</i> intracellularly by the ROS - NLRP3 signalling pathway. The results enrich the understanding of the mechanisms of canine corneal ulcers and facilitate the development of new medicines and prevention measures.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10984133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140185674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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