Yersinia infections

耶尔森氏菌感染
  • 文章类型: Journal Article
    宿主细胞的病原体感染通过炎性半胱天冬酶的激活引发称为焦亡的炎性细胞死亡。然而,耶尔森氏菌毒力因子YopJ对免疫信号激酶的阻断引发细胞死亡,涉及凋亡的caspase-8和焦转的caspase-1。虽然caspase-1通常在炎症体内被激活,耶尔森氏菌诱导的caspase-1激活与已知的炎性体成分无关。我们报道caspase-8是一种重要的引发剂,而caspase-1是通过两个前馈环激活其自身激活的必需放大器,这两个前馈环涉及caspase-1自动加工和caspase-1依赖性GasderminD和NLPR3的激活。值得注意的是,而耶尔森氏菌诱导的caspase-1激活和细胞死亡是不依赖炎性体的,IL-1β释放需要NLPR3炎性体激活。机械上,caspase-8在整个细胞的多个病灶内迅速激活,然后是一个典型的炎症斑点,表明caspase-8和典型的炎性体复合物组件在动力学和空间上是不同的。我们的发现表明,功能上相互关联但不同的死亡复合物介导了对病原体阻断免疫信号的反应,从而介导了焦亡和IL-1β的释放。
    Pathogen infection of host cells triggers an inflammatory cell death termed pyroptosis via activation of inflammatory caspases. However, blockade of immune signaling kinases by the Yersinia virulence factor YopJ triggers cell death involving both apoptotic caspase-8 and pyroptotic caspase-1. While caspase-1 is normally activated within inflammasomes, Yersinia-induced caspase-1 activation is independent of known inflammasome components. We report that caspase-8 is an essential initiator, while caspase-1 is an essential amplifier of its own activation through two feed-forward loops involving caspase-1 auto-processing and caspase-1-dependent activation of gasdermin D and NLPR3. Notably, while Yersinia-induced caspase-1 activation and cell death are inflammasome-independent, IL-1β release requires NLPR3 inflammasome activation. Mechanistically, caspase-8 is rapidly activated within multiple foci throughout the cell, followed by assembly of a canonical inflammasome speck, indicating that caspase-8 and canonical inflammasome complex assemblies are kinetically and spatially distinct. Our findings reveal that functionally interconnected but distinct death complexes mediate pyroptosis and IL-1β release in response to pathogen blockade of immune signaling.
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  • 文章类型: Journal Article
    小肠结肠炎耶尔森氏菌(Y.小肠结肠炎)是耶尔森氏菌病最常见的病因,并在挪威和其他地方引起了几次全国性的暴发。一种标准化的高分辨率方法,如核心基因组多位点序列分型(cgMLST),在国家和国际层面上需要病原体的可追溯性。在这项研究中,我们为小肠结肠炎Y开发并实施了cgMLST方案。我们在SeqSphere中设计了一个cgMLST方案,使用来自不同小肠结肠炎Y生物型亚谱系的高质量基因组。如果在所有测试的小肠结肠炎Y中发现了超过95%的目标,则该方案得到了验证:2012年至2022年之间收集的563个挪威基因组和来自公共数据集的327个基因组。我们将该方案应用于已知的爆发,以根据等位基因差异的数量建立识别主要复杂类型(CT)的阈值。最终的cgMLST方案包括2,582个基因,在所有测试的基因组中发现的目标中位数为97.9%(四分位距97.6%-98.8%)。爆发分析使用四个等位基因差异的单连锁聚类确定了所有爆发菌株。这个阈值确定了挪威的311个独特的CT,其中CT18,CT12和CT5被确定为最常见的与疾病暴发相关.cgMLST方案在使用不同的数据源键入小肠结肠炎Y方面表现出非常好的性能,并且能够识别爆发集群。我们建议在国内和国际上实施该计划,以促进小肠结肠炎的监测,并改善国家和跨境疫情的疫情应对。
    Yersinia enterocolitica (Y. enterocolitica) is the most frequent etiological agent of yersiniosis and has been responsible for several national outbreaks in Norway and elsewhere. A standardized high-resolution method, such as core genome Multilocus Sequence Typing (cgMLST), is needed for pathogen traceability at the national and international levels. In this study, we developed and implemented a cgMLST scheme for Y. enterocolitica. We designed a cgMLST scheme in SeqSphere + using high-quality genomes from different Y. enterocolitica biotype sublineages. The scheme was validated if more than 95% of targets were found across all tested Y. enterocolitica: 563 Norwegian genomes collected between 2012 and 2022 and 327 genomes from public data sets. We applied the scheme to known outbreaks to establish a threshold for identifying major complex types (CTs) based on the number of allelic differences. The final cgMLST scheme included 2,582 genes with a median of 97.9% (interquartile range 97.6%-98.8%) targets found across all tested genomes. Analysis of outbreaks identified all outbreak strains using single linkage clustering at four allelic differences. This threshold identified 311 unique CTs in Norway, of which CT18, CT12, and CT5 were identified as the most frequently associated with outbreaks. The cgMLST scheme showed a very good performance in typing Y. enterocolitica using diverse data sources and was able to identify outbreak clusters. We recommend the implementation of this scheme nationally and internationally to facilitate Y. enterocolitica surveillance and improve outbreak response in national and cross-border outbreaks.
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  • 文章类型: Journal Article
    虹鳟鱼是秘鲁手工水产养殖的重要鱼类,占水产养殖总产量的60%以上。然而,他们的行业受到了诸如耶尔森氏菌等几种细菌制剂的高度影响。这种病原体是肠道红嘴病的病原体,并导致鱼种的高死亡率和成年虹鳟鱼的慢性感染。迄今为止,虹鳟鱼对Y.ruckeri的免疫反应已经在实验室控制感染研究中得到了很好的研究(即腹膜内感染,浴浸),然而,,在自然感染期间的免疫反应尚未被探索。为了解决这个问题,在这项研究中,35例临床健康的O.mykiss,没有病变或行为变化的证据,32例虹鳟鱼自然感染Y.ruckeri,是从秘鲁中部高地的半集约化养鱼场收集的。为了评估对免疫反应的影响,RT-qPCR,西方印迹,用头部肾脏进行ELISA,脾,脾和皮肤组织来评估相对基因表达和蛋白质水平。我们的结果表明,促炎细胞因子il1b的表达显着增加,tnfa,和il6,以及在所有三个组织中的ifng,以及IL-1β和IFN-γ蛋白水平的增加。抗原呈递的内源性途径显示在防御Y.ruckeri中起关键作用,由于mhc-I的上调,tapasin,和b2m成绩单,感染的虹鳟鱼中Tapasin蛋白水平显着增加。与抗原呈递的外源途径相关的基因在感染的鱼中没有显示出显着的增加,这表明该途径不参与针对这种细胞内病原体的反应。最后,免疫球蛋白IgM和IgT的转录本没有显示出调制,在这项研究中也没有评估蛋白质水平。
    Rainbow trout is an important fish species for Peruvian artisanal aquaculture, comprising over 60 % of the total aquaculture production. However, their industry has been highly affected by several bacterial agents such as Yersinia ruckeri. This pathogen is the causative agent of Enteric Redmouth Disease, and causes high mortality in fingerlings and chronic infection in adult rainbow trout. To date, the immune response of rainbow trout against Y. ruckeri has been well studied in laboratory-controlled infection studies (i.e. intraperitoneal infection, bath immersion), however, the immune response during natural infection has not been explored. To address this, in this study, 35 clinically healthy O. mykiss without evidence of lesions or changes in behavior and 32 rainbow trout naturally infected by Y. ruckeri, were collected from semi-intensive fish farms located in the Central Highlands of Peru. To evaluate the effect on the immune response, RT-qPCR, western blotting, and ELISA were conducted using head kidney, spleen, and skin tissues to evaluate the relative gene expression and protein levels. Our results show a significant increase in the expression of the pro-inflammatory cytokines il1b, tnfa, and il6, as well as ifng in all three tissues, as well as increases in IL-1β and IFN-γ protein levels. The endogenous pathway of antigen presentation showed to play a key role in defense against Y. ruckeri, due to the upregulation of mhc-I, tapasin, and b2m transcripts, and the significant increase of Tapasin protein levels in infected rainbow trout. None of the genes associated with the exogenous pathway of antigen presentation showed a significant increase in infected fish, suggesting that this pathway is not involved in the response against this intracellular pathogen. Finally, the transcripts of immunoglobulins IgM and IgT did not show a modulation, nor were the protein levels evaluated in this study.
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  • 文章类型: Journal Article
    耶尔森氏菌是一个重要的属,包括食源性,人畜共患和病原菌。另一方面,所谓的小肠结肠炎耶尔森氏菌类群的物种尚未得到充分研究,并且大多数特征为非致病性,尽管有一些人类感染的报道。本研究旨在提供耶尔森氏菌(YF)的基因组见解,中间耶尔森氏菌(YI)和全球分离的克里斯滕森耶尔森氏菌(YK)。总共22YF,搜索了20个YI和14个YK基因组的抗菌素抗性基因,质粒,预言,和毒力因子。通过Gegenees和核心基因组多位点序列分型分析了它们的系统基因组相关性。β-内酰胺抗性基因blaTEM-116和五个质粒复制子(pYE854,ColRNAI,在少于五个基因组中检测到ColE10,Col(pHAD28)和IncN3。总共59个预言,耶尔森氏菌属的106个毒力标记,与坚持相关,抗吞噬作用,外泌酶,入侵,铁吸收,蛋白酶,分泌系统和O-抗原,并检测到与其他20个细菌属相关的毒力因子。系统基因组分析显示,物种间的差异很高,并且有四个高度多样化的YF簇。总之,通过对YF的分析获得的结果,YI和YK基因组表明了这些菌株的毒力潜力,这是由于发现的噬菌体和毒力因子的广泛多样性和高频率。系统发育分析能够正确区分这些密切相关的物种,并显示存在不同的遗传亚群。这些数据有助于更好地理解YF,YI和YK毒力相关特征和全球遗传多样性,并加强了对这些被认为是非致病性的小肠结肠炎样物种进行更好表征的需求。
    Yersinia is an important genus comprising foodborne, zoonotic and pathogenic bacteria. On the other hand, species of the so-called group Yersinia enterocolitica-like are understudied and mostly characterized as non-pathogenic, despite of some reports of human infections. The present study aimed to provide genomic insights of Yersinia frederiksenii (YF), Yersinia intermedia (YI) and Yersinia kristensenii (YK) isolated worldwide. A total of 22 YF, 20 YI and 14 YK genomes were searched for antimicrobial resistance genes, plasmids, prophages, and virulence factors. Their phylogenomic relatedness was analyzed by Gegenees and core-genome multi-locus sequence typing. Beta-lactam resistance gene blaTEM-116 and five plasmids replicons (pYE854, ColRNAI, ColE10, Col(pHAD28) and IncN3) were detected in less than five genomes. A total of 59 prophages, 106 virulence markers of the Yersinia genus, associated to adherence, antiphagocytosis, exoenzymes, invasion, iron uptake, proteases, secretion systems and the O-antigen, and virulence factors associated to other 20 bacterial genera were detected. Phylogenomic analysis revealed high inter-species distinction and four highly diverse YF clusters. In conclusion, the results obtained through the analyses of YF, YI and YK genomes suggest the virulence potential of these strains due to the broad diversity and high frequency of prophages and virulence factors found. Phylogenetic analyses were able to correctly distinguish these closely related species and show the presence of different genetic subgroups. These data contributed for a better understanding of YF, YI and YK virulence-associated features and global genetic diversity, and reinforced the need for better characterization of these Y. enterocolitica-like species considered non-pathogenic.
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  • 文章类型: Journal Article
    2022年10月,肠道红口病(ERM)影响了湖北一个农场的中国st。中国,造成大规模死亡。受影响的鱼表现出特征性的红嘴和肠道炎症。调查导致分离出一个突出的细菌菌株,zhx1,来自受影响鱼类的内部器官和肠道。人工感染实验证实了zhx1作为导致死亡的病原体的作用。主要病理表现为变性,坏死,和炎症反应,导致多器官功能障碍和死亡。细菌的全基因组测序确定zhx1为耶尔森氏菌,具有135个耐药基因和443个毒力因子相关基因。zhx1的药敏试验显示对氯霉素和氟苯尼考的敏感性很高,但对其他18种抗菌药物有不同程度的耐药性。鉴定与中国st中ERM相关的病原菌,为有效预防和控制该病奠定了理论基础。
    During October 2022, enteric redmouth disease (ERM) affected Chinese sturgeons at a farm in Hubei, China, causing mass mortality. Affected fish exhibited characteristic red mouth and intestinal inflammation. Investigation led to isolation of a prominent bacterial strain, zhx1, from the internal organs and intestines of affected fish. Artificial infection experiments confirmed the role of zhx1 as the pathogen responsible for the deaths. The primary pathologic manifestations consisted of degeneration, necrosis, and inflammatory reactions, resulting in multiple organ dysfunction and death. Whole-genome sequencing of the bacteria identified zhx1 as Yersinia ruckeri, which possesses 135 drug-resistance genes and 443 virulence factor-related genes. Drug-susceptibility testing of zhx1 demonstrated high sensitivity to chloramphenicol and florfenicol but varying degrees of resistance to 18 other antimicrobial drugs. Identifying the pathogenic bacteria associated with ERM in Chinese sturgeons establishes a theoretical foundation for the effective prevention and control of this disease.
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  • 文章类型: Case Reports
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  • 文章类型: Journal Article
    细菌毒素或效应蛋白对靶蛋白的单-O-糖基化是细菌干扰宿主细胞基本功能的公知机制。相应的糖基转移酶是重要的毒力因子,例如艰难梭菌毒素A和B。我们描述了耶尔森氏菌的两种具有高度序列同一性的糖基转移酶:来自人畜共患病原体小肠结肠炎耶尔森氏菌的YeGT和来自鼠病原体耶尔森氏菌的YkGT。我们表明,两者都通过在酪氨酸残基(RhoA中的Tyr-34)上连接N-乙酰葡糖胺(GlcNAc)来修饰Rho家族蛋白。值得注意的是,这些酶的靶蛋白特异性不同。虽然YeGT修改了RhoA,B和C,YkGT具有更宽的底物谱,不仅可以糖基化Rho,还可以糖基化Rac和Cdc42亚家族蛋白。诱变研究表明,残基177对于该更宽的目标谱是重要的。我们确定了YeGT在无配体状态下缩短了16个N末端残基(sYeGT)并与UDP结合的晶体结构,底物水解的产物。该结构将sYeGT分配给GT-A家族。它与来自毒素的糖基转移酶结构域具有高度的结构相似性。我们还证明,YeGT和YkGT的16个最N末端残基对于使用炭疽毒素的成孔保护性抗原介导的易位到宿主细胞中很重要。介导的引入Hela细胞或YeGT和YkGT的异位表达引起肌动蛋白细胞骨架的形态变化和重新分布。数据表明YeGT和YkGT可能是属于酪氨酸糖基化细菌糖基转移酶家族的细菌效应物。
    Mono-O-glycosylation of target proteins by bacterial toxins or effector proteins is a well-known mechanism by which bacteria interfere with essential functions of host cells. The respective glycosyltransferases are important virulence factors such as the Clostridioides difficile toxins A and B. Here, we describe two glycosyltransferases of Yersinia species that have a high sequence identity: YeGT from the zoonotic pathogen Yersinia enterocolitica and YkGT from the murine pathogen Yersinia kristensenii. We show that both modify Rho family proteins by attachment of GlcNAc at tyrosine residues (Tyr-34 in RhoA). Notably, the enzymes differed in their target protein specificity. While YeGT modified RhoA, B, and C, YkGT possessed a broader substrate spectrum and glycosylated not only Rho but also Rac and Cdc42 subfamily proteins. Mutagenesis studies indicated that residue 177 is important for this broader target spectrum. We determined the crystal structure of YeGT shortened by 16 residues N terminally (sYeGT) in the ligand-free state and bound to UDP, the product of substrate hydrolysis. The structure assigns sYeGT to the GT-A family. It shares high structural similarity to glycosyltransferase domains from toxins. We also demonstrated that the 16 most N-terminal residues of YeGT and YkGT are important for the mediated translocation into the host cell using the pore-forming protective antigen of anthrax toxin. Mediated introduction into HeLa cells or ectopic expression of YeGT and YkGT caused morphological changes and redistribution of the actin cytoskeleton. The data suggest that YeGT and YkGT are likely bacterial effectors belonging to the family of tyrosine glycosylating bacterial glycosyltransferases.
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  • 文章类型: Journal Article
    为了建立在抗菌药物敏感性试验中产生的数据的含义,有必要制定国际统一的解释标准。目前,尚未针对鱼类病原体耶尔森氏菌易感性研究中产生的数据制定此类标准。这项工作产生了为该物种的易感性数据设定流行病学截止值所需的数据,该数据是使用标准化的圆盘扩散方法产生的,该方法指定使用MuellerHinton琼脂并在22°C下孵育24-28小时。4种抗菌剂的抑制区数据由3个独立实验室生成.汇总来自这些实验室的数据并使用基于统计学的标准化抗性解释进行分析。对于氨苄青霉素,氟苯尼考,土霉素和甲氧苄啶-磺胺甲恶唑通过该分析计算的临界值为≥16,≥23,≥24和≥30mm,分别。提供的证据表明,这4种药物的数据具有足够的数量和质量,相关当局可以使用这些数据来制定国际统一的,Y.ruckeri的一致流行病学截止值。
    In order to establish the meaning of data generated in antimicrobial agent susceptibility tests, it is necessary to develop internationally harmonised interpretive criteria. Currently, such criteria have not been developed for data generated in studies of the susceptibility of the fish pathogen Yersinia ruckeri. This work generated the data that would be required to set epidemiological cut-off values for the susceptibility data of this species that had been generated using a standardised disc diffusion method that specified the use of Mueller Hinton agar and incubation at 22°C for 24-28 h. Using this method, sets of inhibition zones data for 4 antimicrobial agents were generated by 3 independent laboratories. The data from these laboratories were aggregated and analysed using the statistically based normalised resistance interpretation. For ampicillin, florfenicol, oxytetracycline and trimethoprim-sulfamethoxazole the cut-off values calculated by this analysis were ≥16, ≥23, ≥24 and ≥30 mm, respectively. Evidence is presented demonstrating that the data for these 4 agents was of sufficient quantity and quality that they could be used by the relevant authorities to set internationally harmonised, consensus epidemiological cut-off values for Y. ruckeri.
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  • 文章类型: Journal Article
    肠孢子虫病,欧洲第三大最常见的食源性人畜共患病,主要由病原小肠结肠炎耶尔森氏菌引起。在法国,耶尔森氏菌病微生物监测在耶尔森氏菌国家参考实验室(YNRL)进行。自2017年以来,分离株的特征是全基因组测序(WGS),然后是500个基因的耶尔森氏菌-cgMLST。我们在这里报告了2017-2021年期间基于WGS的小肠结肠炎Y分离株监测数据。YNRL表征了7,642Y。小肠结肠炎菌株分布在来自谱系1Aa和1Ab的2,497个非致病性分离株中,和属于8个致病谱系的5145个标本。在病原分离物中,谱系4最常见(87.2%),其次是谱系2/3-9b(10.6%),2/3-5a(1.2%),2/3-9a(0.6%),3-3b,3-3c,1B,和3-3d(每个0.1%)。重要的是,我们基于一种新的分型方法开发了一种常规监测系统,该方法包括对小肠结肠炎Y种具有特异性的1,727个基因核心基因组多位点序列分型(cgMLST),然后进行分离聚类。确定并固定了分离株聚类的等位基因距离(AD)阈值:谱系4、2/3-5a的AD≤5,和2/3-9a,谱系2/3-9b的AD≤3。2019年在常规监测中实施了聚类计划,以检测致病性分离株的基因组聚类。总的来说,确定了至少2个分离株的419个簇,代表2019年至2021年间表征的3,503株分离株中的2,504株。大多数簇(n=325)包含2至5个分离物。新的分型方法被证明可用于异常病例分组的分子研究以及常规监测中基因组簇的检测。
    目的:我们在这里描述了用于法国小肠结肠炎耶尔森氏菌感染的分子监测的新分型方法,该方法基于对小肠结肠炎耶尔森氏菌特异的新型核心基因组多位点序列分型(cgMLST)物种。该方法可以可靠地鉴定致病性小肠结肠炎耶氏亚种,并以较高的鉴别力比较分离株。在2017年至2021年之间,鉴定了属于8个谱系的5,145个致病性分离株,到目前为止,谱系4是最常见的,其次是谱系2/3-9b。实现了一个聚类程序,和检测阈值通过对三个不寻常的小肠结肠炎耶氏球菌感染组的分子和流行病学调查进行交叉验证。常规的分子监测系统已经能够检测基因组簇,导致流行病学调查。
    Enteric yersiniosis, the third most common food-borne zoonosis in Europe, is mainly caused by the pathogen Yersinia enterocolitica. In France, the yersiniosis microbiological surveillance is conducted at the Yersinia National Reference Laboratory (YNRL). Since 2017, isolates have been characterized by whole genome sequencing (WGS) followed by a 500-gene Yersinia-cgMLST. We report here the data of the WGS-based surveillance on Y. enterocolitica isolates for the 2017-2021 period. The YNRL characterized 7,642 Y. enterocolitica strains distributed in 2,497 non-pathogenic isolates from lineages 1Aa and 1Ab, and 5,145 specimens belonging to 8 pathogenic lineages. Among pathogenic isolates, lineage 4 was the most common (87.2%) followed by lineages 2/3-9b (10.6%), 2/3-5a (1.2%), 2/3-9a (0.6%), 3-3b, 3-3c, 1B, and 3-3d (0.1% per each). Importantly, we developed a routine surveillance system based on a new typing method consisting of a 1,727-genes core genome Multilocus Sequence Typing (cgMLST) specific to the species Y. enterocolitica followed by isolate clustering. Thresholds of allelic distances (AD) were determined and fixed for the clustering of isolates: AD ≤ 5 for lineages 4, 2/3-5a, and 2/3-9a, and AD ≤ 3 for lineage 2/3-9b. Clustering programs were implemented in 2019 in routine surveillance to detect genomic clusters of pathogenic isolates. In total, 419 clusters with at least 2 isolates were identified, representing 2,504 of the 3,503 isolates characterized between 2019 and 2021. Most clusters (n = 325) comprised 2 to 5 isolates. The new typing method proved to be useful for the molecular investigation of unusual grouping of cases as well as for the detection of genomic clusters in routine surveillance.
    OBJECTIVE: We describe here the new typing method used for molecular surveillance of Yersinia enterocolitica infections in France based on a novel core genome Multilocus Sequence Typing (cgMLST) specific to Y. enterocolitica species. This method can reliably identify the pathogenic Y. enterocolitica subspecies and compare the isolates with a high discriminatory power. Between 2017 and 2021, 5,145 pathogenic isolates belonging to 8 lineages were characterized and lineage 4 was by far the most common followed by lineage 2/3-9b. A clustering program was implemented, and detection thresholds were cross-validated by the molecular and epidemiological investigation of three unusual groups of Y. enterocolitica infections. The routine molecular surveillance system has been able to detect genomic clusters, leading to epidemiological investigations.
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    牛肝菌感染引起中华民国肠炎的机制尚不清楚,药物预防和控制措施不仅效果不佳,而且还困扰着许多问题。我们进行了转录组学和16SrRNA测序分析,以检查Y.ruckeri感染和氟苯尼考干预前后杂种st的肠道差异。我们的发现表明Y.ruckeri诱导多种炎症因子的表达,包括IL1β,il6和各种趋化因子,以及casp3,casp8和多个肿瘤坏死因子家族成员,对身体造成病理性伤害。此外,在门的水平,Firmicutes和拟杆菌的相对丰度增加,而在属水平上,泛单胞菌属和环菌属的丰度下降,改变肠道菌群的组成。氟苯尼考干预后,多个细胞凋亡和炎症相关基因表达下调,促进组织修复。然而,植物区系进一步失调,增加感染的风险。总之,我们对转录组和肠道微生物组成的分析表明,Y.ruckeri通过触发细胞凋亡和改变肠道微生物组成来诱导肠道病理损伤。氟苯尼考干预可修复病理损伤,但它也加剧了菌群失衡,导致更高的感染风险。这些发现有助于阐明Y.ruckeri引起的st鱼肠炎的分子机制,并评估药物对st鱼肠道炎症的治疗作用。
    The mechanism by which Y. ruckeri infection induces enteritis in Chinese sturgeon remains unclear, and the efficacy of drug prevention and control measures is not only poor but also plagued with numerous issues. We conducted transcriptomic and 16 S rRNA sequencing analyses to examine the differences in the intestinal tract of hybrid sturgeon before and after Y. ruckeri infection and florfenicol intervention. Our findings revealed that Y. ruckeri induced the expression of multiple inflammatory factors, including il1β, il6, and various chemokines, as well as casp3, casp8, and multiple tumor necrosis factor family members, resulting in pathological injury to the body. Additionally, at the phylum level, the relative abundance of Firmicutes and Bacteroidota increased, while the abundance of Plesiomonas and Cetobacterium decreased at the genus level, altering the composition of the intestinal flora. Following florfenicol intervention, the expression of multiple apoptosis and inflammation-related genes was down-regulated, promoting tissue repair. However, the flora became further dysregulated, increasing the risk of infection. In conclusion, our analysis of the transcriptome and intestinal microbial composition demonstrated that Y. ruckeri induces intestinal pathological damage by triggering apoptosis and altering the composition of the intestinal microbiota. Florfenicol intervention can repair pathological damage, but it also exacerbates flora imbalance, leading to a higher risk of infection. These findings help elucidate the molecular mechanism of Y. ruckeri-induced enteritis in sturgeon and evaluate the therapeutic effect of drugs on intestinal inflammation in sturgeon.
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