Virulence最新文献

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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
{"title":"Pathogenicity and virulence of African swine fever virus.","authors":"Ines Ruedas-Torres, Bui Thi To Nga, Francisco J Salguero","doi":"10.1080/21505594.2024.2375550","DOIUrl":"10.1080/21505594.2024.2375550","url":null,"abstract":"<p><p>African swine fever (ASF) is a devastating disease with a high impact on the pork industry worldwide. ASF virus (ASFV) is a very complex pathogen, the sole member of the family <i>Asfaviridae</i>, which induces a state of immune suppression in the host through infection of myeloid cells and apoptosis of lymphocytes. Moreover, haemorrhages are the other main pathogenic effect of ASFV infection in pigs, related to the infection of endothelial cells, as well as the activation and structural changes of this cell population by proinflammatory cytokine upregulation within bystander monocytes and macrophages. There are still many gaps in the knowledge of the role of proteins produced by the ASFV, which is related to the difficulty in producing a safe and effective vaccine to combat the disease, although few candidates have been approved for use in Southeast Asia in the past couple of years.</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/PMC11232652/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141555610","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
LGG promotes activation of intestinal ILC3 through TLR2 receptor and inhibits salmonella typhimurium infection in mice. LGG 通过 TLR2 受体促进肠道 ILC3 的活化,抑制小鼠鼠伤寒沙门氏菌感染。
IF 5.5 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-07-30 DOI: 10.1080/21505594.2024.2384553
Junhong Wang, Ming Gao, Jiarui Wang, Yan Zeng, Chunfeng Wang, Xin Cao
{"title":"<i>LGG</i> promotes activation of intestinal ILC3 through TLR2 receptor and inhibits <i>salmonella typhimurium</i> infection in mice.","authors":"Junhong Wang, Ming Gao, Jiarui Wang, Yan Zeng, Chunfeng Wang, Xin Cao","doi":"10.1080/21505594.2024.2384553","DOIUrl":"10.1080/21505594.2024.2384553","url":null,"abstract":"<p><p><i>Salmonella</i> is a foodborne pathogen that causes disruption of intestinal mucosal immunity, leading to acute gastroenteritis in the host. In this study, we found that <i>Salmonella Typhimurium</i> (<i>STM</i>) infection of the intestinal tract of mice led to a significant increase in the proportion of <i>Lacticaseibacillus</i>, while the secretion of IL-22 from type 3 innate lymphoid cells (ILC3) increased significantly. Feeding <i>Lacticaseibacillus rhamnosus GG</i> (<i>LGG</i>) effectively alleviated the infection of <i>STM</i> in the mouse intestines. TLR2<sup>-/-</sup> mice experiments found that TLR2-expressing dendritic cells (DCs) are crucial for <i>LGG</i>'s activation of ILC3. Subsequent in vitro experiments showed that heat-killed <i>LGG</i> (HK<i>-LGG</i>) could promote DCs to secrete IL-23, which in turn further promotes the activation of ILC3 and the secretion of IL-22. Finally, organoid experiments further verified that IL-22 secreted by ILC3 can enhance the intestinal mucosal immune barrier and inhibit <i>STM</i> infection. This study demonstrates that oral administration of <i>LGG</i> is a potential method for inhibiting <i>STM</i> infection.</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/PMC11296546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141856635","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
Correction. 更正。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-06-09 DOI: 10.1080/21505594.2024.2363658
{"title":"Correction.","authors":"","doi":"10.1080/21505594.2024.2363658","DOIUrl":"10.1080/21505594.2024.2363658","url":null,"abstract":"","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/PMC11168232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141296879","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
M1-type polarized macrophage contributes to brain damage through CXCR3.2/CXCL11 pathways after RGNNV infection in grouper. 石斑鱼感染 RGNNV 后,M1 型极化巨噬细胞通过 CXCR3.2/CXCL11 途径造成脑损伤。
IF 5.2 1区 农林科学
Virulence Pub Date : 2024-12-01 Epub Date: 2024-05-23 DOI: 10.1080/21505594.2024.2355971
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
{"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":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/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}
引用次数: 0
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