Virulence最新文献

{"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":" ","pages":"2412745"},"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}

{"title":"M1-type polarized macrophage contributes to brain damage through CXCR3.2/CXCL11 pathways after RGNNV infection in grouper.","authors":"Kaishan Liang, Minlin Zhang, Jiantao Liang, Xiaoling Zuo, Xianze Jia, Jinhong Shan, Zongyang Li, Jie Yu, Zijie Xuan, Liyuan Luo, Huihong Zhao, Songyong Gan, Ding Liu, Qiwei Qin, Qing Wang","doi":"10.1080/21505594.2024.2355971","DOIUrl":"10.1080/21505594.2024.2355971","url":null,"abstract":"<p><p>The vertebrate central nervous system (CNS) is the most complex system of the body. The CNS, especially the brain, is generally regarded as immune-privileged. However, the specialized immune strategies in the brain and how immune cells, specifically macrophages in the brain, respond to virus invasion remain poorly understood. Therefore, this study aimed to examine the potential immune response of macrophages in the brain of orange-spotted groupers (<i>Epinephelus coioides</i>) following red-spotted grouper nervous necrosis virus (RGNNV) infection. We observed that RGNNV induced macrophages to produce an inflammatory response in the brain of orange-spotted grouper, and the macrophages exhibited M1-type polarization after RGNNV infection. In addition, we found RGNNV-induced macrophage M1 polarization via the CXCR3.2- CXCL11 pathway. Furthermore, we observed that RGNNV triggered M1 polarization in macrophages, resulting in substantial proinflammatory cytokine production and subsequent damage to brain tissue. These findings reveal a unique mechanism for brain macrophage polarization, emphasizing their role in contributing to nervous tissue damage following viral infection in the CNS.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":" ","pages":"2355971"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11123556/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140923264","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}

{"title":"Outer membrane vesicles from genetically engineered <i>Salmonella enterica</i> serovar Typhimurium presenting <i>Helicobacter pylori</i> antigens UreB and CagA induce protection against <i>Helicobacter pylori</i> infection in mice.","authors":"Qiong Liu, Yinpan Shang, Lu Shen, Xiaomin Yu, Yanli Cao, Lingbing Zeng, Hanchi Zhang, Zirong Rao, Yi Li, Ziwei Tao, Zhili Liu, Xiaotian Huang","doi":"10.1080/21505594.2024.2367783","DOIUrl":"10.1080/21505594.2024.2367783","url":null,"abstract":"<p><p><i>Helicobacter pylori</i> causes globally prevalent infections that are highly related to chronic gastritis and even development of gastric carcinomas. With the increase of antibiotic resistance, scientists have begun to search for better vaccine design strategies to eradicate <i>H. pylori</i> colonization. However, while current strategies prefer to formulate vaccines with a single <i>H. pylori</i> antigen, their potential has not yet been fully realized. Outer membrane vesicles (OMVs) are a potential platform since they could deliver multiple antigens. In this study, we engineered three crucial <i>H. pylori</i> antigen proteins (UreB, CagA, and VacA) onto the surface of OMVs derived from <i>Salmonella enterica</i> serovar Typhimurium (<i>S</i>. Typhimurium) mutant strains using the hemoglobin protease (Hbp) autotransporter system. In various knockout strategies, we found that OMVs isolated from the Δ<i>rfbP</i> Δ<i>fliC</i> Δ<i>fljB</i> Δ<i>ompA</i> mutants could cause distinct increases in immunoglobulin G (IgG) and A (IgA) levels and effectively trigger T helper 1- and 17-biased cellular immune responses, which perform a vital role in protecting against <i>H. pylori</i>. Next, OMVs derived from Δ<i>rfbP</i> Δ<i>fliC</i> Δ<i>fljB</i> Δ<i>ompA</i> mutants were used as a vector to deliver different combinations of <i>H. pylori</i> antigens. The antibody and cytokine levels and challenge experiments in mice model indicated that co-delivering UreB and CagA could protect against <i>H. pylori</i> and antigen-specific T cell responses. In summary, OMVs derived from the <i>S</i>. Typhimurium Δ<i>rfbP</i> Δ<i>fliC</i> Δ<i>fljB</i> Δ<i>ompA</i> mutant strain as the vector while importing <i>H. pylori</i> UreB and CagA as antigenic proteins using the Hbp autotransporter system would greatly benefit controlling <i>H. pylori</i> infection.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"15 1","pages":"2367783"},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11216100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141471110","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}

{"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":"15 1","pages":"2422539"},"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}

{"title":"In turkeys, unlike chickens, the non-structural NS1 protein does not play a significant role in the replication and tissue tropism of the H7N1 avian influenza virus.","authors":"Maryna Kuryshko, Maria Landmann, Christine Luttermann, Reiner Ulrich, Elsayed M Abdelwhab","doi":"10.1080/21505594.2024.2379371","DOIUrl":"10.1080/21505594.2024.2379371","url":null,"abstract":"<p><p>The economic losses caused by high pathogenicity (HP) avian influenza viruses (AIV) in the poultry industry worldwide are enormous. Although chickens and turkeys are closely related Galliformes, turkeys are thought to be a bridging host for the adaptation of AIV from wild birds to poultry because of their high susceptibility to AIV infections. HPAIV evolve from low pathogenicity (LP) AIV after circulation in poultry through mutations in different viral proteins, including the non-structural protein (NS1), a major interferon (IFN) antagonist of AIV. At present, it is largely unknown whether the virulence determinants of HPAIV are the same in turkeys and chickens. Previously, we showed that mutations in the NS1 of HPAIV H7N1 significantly reduced viral replication in chickens <i>in</i> <i>vitro</i> and <i>in</i> <i>vivo</i>. Here, we investigated the effect of NS1 on the replication and virulence of HPAIV H7N1 in turkeys after inoculation with recombinant H7N1 carrying a naturally truncated wild-type NS1 (with 224 amino-acid \"aa\" in length) or an extended NS1 with 230-aa similar to the LP H7N1 ancestor. There were no significant differences in multiple-cycle viral replication or in the efficiency of NS1 in blocking IFN induction in the cell culture. Similarly, all viruses were highly virulent in turkeys and replicated at similar levels in various organs and swabs collected from the inoculated turkeys. These results suggest that NS1 does not play a role in the virulence or replication of HPAIV H7N1 in turkeys and further indicate that the genetic determinants of HPAIV differ in these two closely related galliform species.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"15 1","pages":"2379371"},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11259080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627821","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}

{"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 A¹¹². 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":" ","pages":"2421219"},"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}

{"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":" ","pages":"2421983"},"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}

{"title":"Study of the relationships among known virulence genes, coccoid transformation and cytotoxicity of <i>Helicobacter pylori</i> in different clinical diseases.","authors":"Yao Xiao, Binghua Zhang, Huifang Zhang, Zehui Zhang, Fanliang Meng, Xin Zhao, Jianzhong Zhang, Di Xiao","doi":"10.1080/21505594.2024.2418407","DOIUrl":"10.1080/21505594.2024.2418407","url":null,"abstract":"<p><strong>Background: </strong><i>Helicobacter pylori (H. pylori)</i> has infected approximately 4.4 billion individuals worldwide. The known virulence genes and the existing <i>H. pylori</i> typing methods have not been shown to have a recognized correlation with its infectivity. The aim of this study was to elucidate the relationships among known important virulence genes, coccoid transformation, and cytotoxicity of <i>H. pylori</i> isolated from individuals with different clinical diseases to provide guidance for the development of new virulence typing methods for <i>H. pylori</i>.</p><p><strong>Methods: </strong>The known important virulence genes of 35 <i>H. pylori</i> strains were identified by whole-gene next-generation sequencing (WGS) and polymerase chain reaction (PCR). The chronological changes in the proportion of coccoid forms of <i>H. pylori</i> and their ultramicroscopic structures were observed chronologically using transmission electron microscopy. Human gastric mucosal epithelial cells (GES-1) were infected with <i>H. pylori</i> strains in vitro to evaluate cytotoxicity of <i>H. pylori</i>.</p><p><strong>Results: </strong>There were no significant correlations among the known important virulence genes, coccoid transformation and cytotoxicity of <i>H. pylori</i> isolated from patients with different clinical diseases. We developed a new virulence classification based on the defensive and offensive abilities of <i>H. pylori</i>.</p><p><strong>Conclusions: </strong>Coccoid transformation and virulence are two independent characteristics of <i>H. pylori</i> that reflect its defensive and offensive abilities, respectively. These two abilities work synergistically, warranting the construction of a new virulence typing method for <i>H. pylori</i>. However, the correlation between the new virulence classification and pathogenic ability still needs to be further verified.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"15 1","pages":"2418407"},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11497995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142476127","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}

{"title":"Hijacking host cell vesicular transport: New insights into the nutrient acquisition mechanism of <i>Chlamydia</i>.","authors":"Lei Wenbo, Yang Yewei, Zhou Hui, Li Zhongyu","doi":"10.1080/21505594.2024.2351234","DOIUrl":"10.1080/21505594.2024.2351234","url":null,"abstract":"<p><p><i>Chlamydia</i> infection is an important cause of public health diseases, and no effective vaccine is currently available. Owing to its unique intracellular lifestyle, <i>Chlamydia</i> requires a variety of nutrients and substrates from host cells, particularly sphingomyelin, cholesterol, iron, amino acids, and the mannose-6-phosphate receptor, which are essential for inclusion development. Here, we summarize the recent advances in <i>Chlamydia</i> nutrient acquisition mechanism by hijacking host cell vesicular transport, which plays an important role in chlamydial growth and development. <i>Chlamydia</i> obtains the components necessary to complete its intracellular developmental cycle by recruiting Rab proteins (major vesicular trafficking regulators) and Rab effector proteins to the inclusion, interfering with Rab-mediated multivesicular trafficking, reorienting the nutrition of host cells, and reconstructing the intracellular niche environment. Consequently, exploring the role of vesicular transport in nutrient acquisition offers a novel perspective on new approaches for preventing and treating <i>Chlamydia</i> infection.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"15 1","pages":"2351234"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11123459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141076901","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}

{"title":"Integrative and conjugative elements of <i>Pasteurella multocida</i>: Prevalence and signatures in population evolution.","authors":"Jiao He, Zhishuang Yang, Mingshu Wang, Renyong Jia, Shun Chen, Mafeng Liu, Xinxin Zhao, Qiao Yang, Ying Wu, Shaqiu Zhang, Juan Huang, Xumin Ou, Di Sun, Bin Tian, Yu He, Zhen Wu, Anchun Cheng, Dekang Zhu","doi":"10.1080/21505594.2024.2359467","DOIUrl":"10.1080/21505594.2024.2359467","url":null,"abstract":"<p><p><i>Pasteurella multocida</i> (<i>P. multocida</i>) is a bacterial pathogen responsible for a range of infections in humans and various animal hosts, causing significant economic losses in farming. Integrative and conjugative elements (ICEs) are important horizontal gene transfer elements, potentially enabling host bacteria to enhance adaptability by acquiring multiple functional genes. However, the understanding of ICEs in <i>P. multocida</i> and their impact on the transmission of this pathogen remains limited. In this study, 42 poultry-sourced <i>P. multocida</i> genomes obtained by high-throughput sequencing together with 393 publicly available <i>P. multocida</i> genomes were used to analyse the horizontal transfer of ICEs. Eighty-two ICEs were identified in <i>P. multocida</i>, including SXT/R391 and Tn916 subtypes, as well as three subtypes of ICE<i>Hin</i>1056 family, with the latter being widely prevalent in <i>P. multocida</i> and carrying multiple resistance genes. The correlations between insertion sequences and resistant genes in ICEs were also identified, and some ICEs introduced the carbapenem gene <i>bla</i>_OXA-2 and the bleomycin gene <i>bleO</i> to <i>P. multocida</i>. Phylogenetic and collinearity analyses of these bioinformatics found that ICEs in <i>P. multocida</i> were transmitted vertically and horizontally and have evolved with host specialization. These findings provide insight into the transmission and evolution mode of ICEs in <i>P. multocida</i> and highlight the importance of understanding these elements for controlling the spread of antibiotic resistance.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"15 1","pages":"2359467"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11141479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161392","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}