Virulence最新文献

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The pathogenicity and virulence of the opportunistic pathogen Staphylococcus epidermidis. 机会性病原体表皮葡萄球菌的致病性和毒性。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-06-13 DOI: 10.1080/21505594.2024.2359483
Órla Burke, Merve S Zeden, James P O'Gara
{"title":"The pathogenicity and virulence of the opportunistic pathogen <i>Staphylococcus epidermidis</i>.","authors":"Órla Burke, Merve S Zeden, James P O'Gara","doi":"10.1080/21505594.2024.2359483","DOIUrl":"10.1080/21505594.2024.2359483","url":null,"abstract":"<p><p>The pervasive presence of <i>Staphylococcus epidermidis</i> and other coagulase-negative staphylococci on the skin and mucous membranes has long underpinned a casual disregard for the infection risk that these organisms pose to vulnerable patients in healthcare settings. Prior to the recognition of biofilm as an important virulence determinant in <i>S. epidermidis</i>, isolation of this microorganism in diagnostic specimens was often overlooked as clinically insignificant with potential delays in diagnosis and onset of appropriate treatment, contributing to the establishment of chronic infection and increased morbidity or mortality. While impressive progress has been made in our understanding of biofilm mechanisms in this important opportunistic pathogen, research into other virulence determinants has lagged <i>S. aureus</i>. In this review, the broader virulence potential of <i>S. epidermidis</i> including biofilm, toxins, proteases, immune evasion strategies and antibiotic resistance mechanisms is surveyed, together with current and future approaches for improved therapeutic interventions.</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/PMC11178275/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141311939","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
Exogenous NADH promotes the bactericidal effect of aminoglycoside antibiotics against Edwardsiella tarda. 外源性 NADH 可促进氨基糖苷类抗生素对arda Edwardsiella 的杀菌作用。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-06-17 DOI: 10.1080/21505594.2024.2367647
Yilin Zhong, Juan Guo, Ziyi Zhang, Yu Zheng, Manjun Yang, Yubin Su
{"title":"Exogenous NADH promotes the bactericidal effect of aminoglycoside antibiotics against <i>Edwardsiella tarda</i>.","authors":"Yilin Zhong, Juan Guo, Ziyi Zhang, Yu Zheng, Manjun Yang, Yubin Su","doi":"10.1080/21505594.2024.2367647","DOIUrl":"10.1080/21505594.2024.2367647","url":null,"abstract":"<p><p>The global surge in multidrug-resistant bacteria owing to antibiotic misuse and overuse poses considerable risks to human and animal health. With existing antibiotics losing their effectiveness and the protracted process of developing new antibiotics, urgent alternatives are imperative to curb disease spread. Notably, improving the bactericidal effect of antibiotics by using non-antibiotic substances has emerged as a viable strategy. Although reduced nicotinamide adenine dinucleotide (NADH) may play a crucial role in regulating bacterial resistance, studies examining how the change of metabolic profile and bacterial resistance following by exogenous administration are scarce. Therefore, this study aimed to elucidate the metabolic changes that occur in <i>Edwardsiella tarda</i> (<i>E. tarda</i>), which exhibits resistance to various antibiotics, following the exogenous addition of NADH using metabolomics. The effects of these alterations on the bactericidal activity of neomycin were investigated. NADH enhanced the effectiveness of aminoglycoside antibiotics against <i>E. tarda</i> ATCC15947, achieving bacterial eradication at low doses. Metabolomic analysis revealed that NADH reprogrammed the ATCC15947 metabolic profile by promoting purine metabolism and energy metabolism, yielding increased adenosine triphosphate (ATP) levels. Increased ATP levels played a crucial role in enhancing the bactericidal effects of neomycin. Moreover, exogenous NADH promoted the bactericidal efficacy of tetracyclines and chloramphenicols. NADH in combination with neomycin was effective against other clinically resistant bacteria, including <i>Aeromonas hydrophila, Vibrio parahaemolyticus</i>, methicillin-resistant <i>Staphylococcus aureus</i>, and <i>Listeria monocytogenes</i>. These results may facilitate the development of effective approaches for preventing and managing <i>E. tarda</i>-induced infections and multidrug resistance in aquaculture and clinical settings.</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/PMC11185186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141331919","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
Streptococcal arginine deiminase system defences macrophage bactericidal effect mediated by XRE family protein XtrSs. 链球菌精氨酸脱氨酶系统通过 XRE 家族蛋白 XtrSs 的介导,抵御巨噬细胞的杀菌作用。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-02-02 DOI: 10.1080/21505594.2024.2306719
Yumin Zhang, Song Liang, Shidan Zhang, Qiankun Bai, Lei Dai, Jinxiu Wang, Huochun Yao, Wei Zhang, Guangjin Liu
{"title":"Streptococcal arginine deiminase system defences macrophage bactericidal effect mediated by XRE family protein XtrSs.","authors":"Yumin Zhang, Song Liang, Shidan Zhang, Qiankun Bai, Lei Dai, Jinxiu Wang, Huochun Yao, Wei Zhang, Guangjin Liu","doi":"10.1080/21505594.2024.2306719","DOIUrl":"10.1080/21505594.2024.2306719","url":null,"abstract":"<p><p>The arginine deiminase system (ADS) has been identified in various bacteria and functions to supplement energy production and enhance biological adaptability. The current understanding of the regulatory mechanism of ADS and its effect on bacterial pathogenesis is still limited. Here, we found that the XRE family transcriptional regulator XtrSs negatively affected <i>Streptococcus suis</i> virulence and significantly repressed ADS transcription when the bacteria were incubated in blood. Electrophoretic mobility shift (EMSA) and lacZ fusion assays further showed that XtrSs directly bind to the promoter of ArgR, an acknowledged positive regulator of bacterial ADS, to repress ArgR transcription. Moreover, we provided compelling evidence that <i>S. suis</i> could utilize arginine via ADS to adapt to acid stress, while Δ<i>xtrSs</i> enhanced this acid resistance by upregulating the ADS operon. Moreover, whole ADS-knockout <i>S. suis</i> increased arginine and antimicrobial NO in the infected macrophage cells, decreased intracellular survival, and even caused significant attenuation of bacterial virulence in a mouse infection model, while Δ<i>xtrSs</i> consistently presented the opposite results. Our experiments identified a novel ADS regulatory mechanism in <i>S. suis</i>, whereby XtrSs regulated ADS to modulate NO content in macrophages, promoting <i>S. suis</i> intracellular survival. Meanwhile, our findings provide a new perspective on how <i>Streptococci</i> evade the host's innate immune system.</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/PMC10841013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139513787","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
Coxiella burnetii effector CvpE maintains biogenesis of Coxiella-containing vacuoles by suppressing lysosome tubulation through binding PI(3)P and perturbing PIKfyve activity on lysosomes. 烧伤柯西氏菌效应子 CvpE 通过结合 PI(3)P 和扰乱溶酶体上 PIKfyve 的活性抑制溶酶体管化,从而维持含柯西氏菌空泡的生物生成。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-05-09 DOI: 10.1080/21505594.2024.2350893
Mingliang Zhao, Shan Zhang, Weiqiang Wan, Chunyu Zhou, Nana Li, Ruxi Cheng, Yonghui Yu, Xuan Ouyang, Dongsheng Zhou, Jun Jiao, Xiaolu Xiong
{"title":"<i>Coxiella burnetii</i> effector CvpE maintains biogenesis of <i>Coxiella</i>-containing vacuoles by suppressing lysosome tubulation through binding PI(3)P and perturbing PIKfyve activity on lysosomes.","authors":"Mingliang Zhao, Shan Zhang, Weiqiang Wan, Chunyu Zhou, Nana Li, Ruxi Cheng, Yonghui Yu, Xuan Ouyang, Dongsheng Zhou, Jun Jiao, Xiaolu Xiong","doi":"10.1080/21505594.2024.2350893","DOIUrl":"10.1080/21505594.2024.2350893","url":null,"abstract":"<p><p><i>Coxiella burnetii</i> (<i>C. burnetii</i>) is the causative agent of Q fever, a zoonotic disease. Intracellular replication of <i>C. burnetii</i> requires the maturation of a phagolysosome-like compartment known as the replication permissive <i>Coxiella</i>-containing vacuole (CCV). Effector proteins secreted by the Dot/Icm secretion system are indispensable for maturation of a single large CCV by facilitating the fusion of promiscuous vesicles. However, the mechanisms of CCV maintenance and evasion of host cell clearance remain to be defined. Here, we show that <i>C. burnetii</i> secreted <i>Coxiella</i> vacuolar protein E (CvpE) contributes to CCV biogenesis by inducing lysosome-like vacuole (LLV) enlargement. LLV fission by tubulation and autolysosome degradation is impaired in CvpE-expressing cells. Subsequently, we found that CvpE suppresses lysosomal Ca<sup>2+</sup> channel transient receptor potential channel mucolipin 1 (TRPML1) activity in an indirect manner, in which CvpE binds phosphatidylinositol 3-phosphate [PI(3)P] and perturbs PIKfyve activity in lysosomes. Finally, the agonist of TRPML1, ML-SA5, inhibits CCV biogenesis and <i>C. burnetii</i> replication. These results provide insight into the mechanisms of CCV maintenance by CvpE and suggest that the agonist of TRPML1 can be a novel potential treatment that does not rely on antibiotics for Q fever by enhancing Coxiella-containing vacuoles (CCVs) fission.</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/PMC11085968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899204","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
Alpha1-antitrypsin impacts innate host-pathogen interactions with Candida albicans by stimulating fungal filamentation. α1-抗胰蛋白酶通过刺激真菌丝状化影响宿主-病原体与白色念珠菌的先天相互作用。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-04-10 DOI: 10.1080/21505594.2024.2333367
Martin Jaeger, Axel Dietschmann, Sophie Austermeier, Sude Dinçer, Pauline Porschitz, Larsen Vornholz, Ralph J A Maas, Evelien G G Sprenkeler, Jürgen Ruland, Stefan Wirtz, Tania Azam, Leo A B Joosten, Bernhard Hube, Mihai G Netea, Charles A Dinarello, Mark S Gresnigt
{"title":"Alpha1-antitrypsin impacts innate host-pathogen interactions with <i>Candida albicans</i> by stimulating fungal filamentation.","authors":"Martin Jaeger, Axel Dietschmann, Sophie Austermeier, Sude Dinçer, Pauline Porschitz, Larsen Vornholz, Ralph J A Maas, Evelien G G Sprenkeler, Jürgen Ruland, Stefan Wirtz, Tania Azam, Leo A B Joosten, Bernhard Hube, Mihai G Netea, Charles A Dinarello, Mark S Gresnigt","doi":"10.1080/21505594.2024.2333367","DOIUrl":"10.1080/21505594.2024.2333367","url":null,"abstract":"<p><p>Our immune system possesses sophisticated mechanisms to cope with invading microorganisms, while pathogens evolve strategies to deal with threats imposed by host immunity. Human plasma protein α1-antitrypsin (AAT) exhibits pleiotropic immune-modulating properties by both preventing immunopathology and improving antimicrobial host defence. Genetic associations suggested a role for AAT in candidemia, the most frequent fungal blood stream infection in intensive care units, yet little is known about how AAT influences interactions between <i>Candida albicans</i> and the immune system. Here, we show that AAT differentially impacts fungal killing by innate phagocytes. We observed that AAT induces fungal transcriptional reprogramming, associated with cell wall remodelling and downregulation of filamentation repressors. At low concentrations, the cell-wall remodelling induced by AAT increased immunogenic β-glucan exposure and consequently improved fungal clearance by monocytes. Contrastingly, higher AAT concentrations led to excessive <i>C. albicans</i> filamentation and thus promoted fungal immune escape from monocytes and macrophages. This underscores that fungal adaptations to the host protein AAT can differentially define the outcome of encounters with innate immune cells, either contributing to improved immune recognition or fungal immune escape.</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/PMC11008552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140185675","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
Gut-brain axis interplay via STAT3 pathway: Implications of Helicobacter pylori derived secretome on inflammation and Alzheimer's disease. 通过 STAT3 通路实现肠道-大脑轴相互作用:幽门螺杆菌分泌物对炎症和阿尔茨海默病的影响
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-02-04 DOI: 10.1080/21505594.2024.2303853
Meenakshi Kandpal, Budhadev Baral, Nidhi Varshney, Ajay Kumar Jain, Debi Chatterji, Ajay Kumar Meena, Rajan Kumar Pandey, Hem Chandra Jha
{"title":"Gut-brain axis interplay via STAT3 pathway: Implications of <i>Helicobacter pylori</i> derived secretome on inflammation and Alzheimer's disease.","authors":"Meenakshi Kandpal, Budhadev Baral, Nidhi Varshney, Ajay Kumar Jain, Debi Chatterji, Ajay Kumar Meena, Rajan Kumar Pandey, Hem Chandra Jha","doi":"10.1080/21505594.2024.2303853","DOIUrl":"10.1080/21505594.2024.2303853","url":null,"abstract":"<p><p><i>Helicobacter pylori</i> is a pathogenic bacterium that causes gastritis and gastric carcinoma. Besides gastric complications its potential link with gut-brain axis disruption and neurological disorders has also been reported. The current study investigated the plausible role and its associated molecular mechanism underlying <i>H. pylori</i> mediated gut-brain axis disruption and neuroinflammation leading to neurological modalities like Alzheimer's disease (AD). We have chosen the antimicrobial resistant and susceptible <i>H. pylori</i> strains on the basis of broth dilution method. We have observed the increased inflammatory response exerted by <i>H. pylori</i> strains in the gastric as well as in the neuronal compartment after treatment with <i>Helicobacter pylori</i> derived condition media (HPCM). Further, elevated expression of STAT1, STAT3, and AD-associated proteins- APP and APOE4 was monitored in HPCM-treated neuronal and neuron-astrocyte co-cultured cells. Excessive ROS generation has been found in these cells. The HPCM treatment to LN229 causes astrogliosis, evidenced by increased glial fibrillary acidic protein. Our results indicate the association of STAT3 as an important regulator in the <i>H. pylori-</i>mediated pathogenesis in neuronal cells. Notably, the inhibition of STAT3 by its specific inhibitor, BP-1-102, reduced the expression of pSTAT3 and AD markers in neuronal compartment induced by HPCM. Thus, our study demonstrates that <i>H. pylori</i> infection exacerbates inflammation in AGS cells and modulates the activity of STAT3 regulatory molecules. <i>H. pylori</i> secretome could affect neurological compartments by promoting STAT3 activation and inducing the expression of AD-associated signature markers. Further, pSTAT-3 inhibition mitigates the <i>H. pylori</i> associated neuroinflammation and amyloid pathology.</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/PMC10854367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139404601","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
Iron depletion has different consequences on the growth and survival of Toxoplasma gondii strains. 铁耗竭对弓形虫菌株的生长和存活有不同的影响。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-03-20 DOI: 10.1080/21505594.2024.2329566
Eléa A Renaud, Ambre J M Maupin, Yann Bordat, Arnault Graindorge, Laurence Berry, Sébastien Besteiro
{"title":"Iron depletion has different consequences on the growth and survival of <i>Toxoplasma gondii</i> strains.","authors":"Eléa A Renaud, Ambre J M Maupin, Yann Bordat, Arnault Graindorge, Laurence Berry, Sébastien Besteiro","doi":"10.1080/21505594.2024.2329566","DOIUrl":"10.1080/21505594.2024.2329566","url":null,"abstract":"<p><p><i>Toxoplasma gondii</i> is an obligate intracellular parasite responsible for a pathology called toxoplasmosis, which primarily affects immunocompromised individuals and developing foetuses. The parasite can scavenge essential nutrients from its host to support its growth and survival. Among them, iron is one of the most important elements needed to sustain basic cellular functions as it is involved in a number of key metabolic processes, including oxygen transport, redox balance, and electron transport. We evaluated the effects of an iron chelator on the development of several parasite strains and found that they differed in their ability to tolerate iron depletion. The growth of parasites usually associated with a model of acute toxoplasmosis was strongly affected by iron depletion, whereas cystogenic strains were less sensitive as they were able to convert into persisting developmental forms that are associated with the chronic form of the disease. Ultrastructural and biochemical characterization of the impact of iron depletion on parasites also highlighted striking changes in both their metabolism and that of the host, with a marked accumulation of lipid droplets and perturbation of lipid homoeostasis. Overall, our study demonstrates that although acute iron depletion has an important effect on the growth of <i>T. gondii</i>, it has a more profound impact on actively dividing parasites, whereas less metabolically active parasite forms may be able to avoid some of the most detrimental consequences.</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/PMC10962585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140176762","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
Pathogenicity and virulence of O'nyong-nyong virus: A less studied Togaviridae with pandemic potential. O'nyong-nyong 病毒的致病性和毒性:一种研究较少但具有大流行潜力的 Togaviridae。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-05-26 DOI: 10.1080/21505594.2024.2355201
Samuel Tong Jia Ming, Katrina Tan Yi Jun, Guillaume Carissimo
{"title":"Pathogenicity and virulence of O'nyong-nyong virus: A less studied <i>Togaviridae</i> with pandemic potential.","authors":"Samuel Tong Jia Ming, Katrina Tan Yi Jun, Guillaume Carissimo","doi":"10.1080/21505594.2024.2355201","DOIUrl":"10.1080/21505594.2024.2355201","url":null,"abstract":"<p><p>O'nyong-nyong virus (ONNV) is a neglected mosquito-borne alphavirus belonging to the <i>Togaviridae</i> family. ONNV is known to be responsible for sporadic outbreaks of acute febrile disease and polyarthralgia in Africa. As climate change increases the geographical range of known and potential new vectors, recent data indicate a possibility for ONNV to spread outside of the African continent and grow into a greater public health concern. In this review, we summarise the current knowledge on ONNV epidemiology, host-pathogen interactions, vector-virus responses, and insights into possible avenues to control risk of further epidemics. In this review, the limited ONNV literature is compared and correlated to other findings on mainly Old World alphaviruses. We highlight and discuss studies that investigate viral and host factors that determine viral-vector specificity, along with important mechanisms that determine severity and disease outcome of ONNV infection.</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/PMC11135837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141155388","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
NagZ modulates the virulence of E. cloacae by acting through the gene of unknown function, ECL_03795. NagZ 通过未知功能基因 ECL_03795 发挥作用,从而调节衣藻埃希氏菌的毒力。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-06-24 DOI: 10.1080/21505594.2024.2367652
Xianggui Yang, Jun Zeng, Dan Wang, Qin Zhou, Xuejing Yu, Zhenguo Wang, Tingting Bai, Guangxin Luan, Ying Xu
{"title":"NagZ modulates the virulence of <i>E. cloacae</i> by acting through the gene of unknown function, ECL_03795.","authors":"Xianggui Yang, Jun Zeng, Dan Wang, Qin Zhou, Xuejing Yu, Zhenguo Wang, Tingting Bai, Guangxin Luan, Ying Xu","doi":"10.1080/21505594.2024.2367652","DOIUrl":"10.1080/21505594.2024.2367652","url":null,"abstract":"<p><p>β-N-acetylglucosaminidase (NagZ), a cytosolic glucosaminidase, plays a pivotal role in peptidoglycan recycling. Previous research demonstrated that NagZ knockout significantly eradicated AmpC-dependent β-lactam resistance in <i>Enterobacter cloacae</i>. However, NagZ's role in the virulence of <i>E. cloacae</i> remains unclear. Our study, incorporating data on mouse and <i>Galleria mellonella</i> larval mortality rates, inflammation markers, and histopathological examinations, revealed a substantial reduction in the virulence of <i>E. cloacae</i> following NagZ knockout. Transcriptome sequencing uncovered differential gene expression between NagZ knockout and wild-type strains, particularly in nucleotide metabolism pathways. Further investigation demonstrated that NagZ deletion led to a significant increase in cyclic diguanosine monophosphate (c-di-GMP) levels. Additionally, transcriptome sequencing and RT-qPCR confirmed significant differences in the expression of ECL_03795, a gene with an unknown function but speculated to be involved in c-di-GMP metabolism due to its EAL domain known for phosphodiesterase activity. Interestingly, in ECL_03795 knockout strains, a notable reduction in the virulence was observed, and virulence was rescued upon complementation with ECL_03795. Consequently, our study suggests that NagZ's function on virulence is partially mediated through the ECL_03795→c-di-GMP pathway, providing insight into the development of novel therapies and strongly supporting the interest in creating highly efficient NagZ inhibitors.</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/PMC11197897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141443403","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
Pathogenicity and virulence of African swine fever virus. 非洲猪瘟病毒的致病性和毒性。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-07-07 DOI: 10.1080/21505594.2024.2375550
Ines Ruedas-Torres, Bui Thi To Nga, Francisco J Salguero
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