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IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-04-09 DOI: 10.1111/1348-0421.13126

Cover photograph: Streptococcus pneumoniae ΔlspA strain induces less SEAP production in THP-1-Blue cells. Microbiol Immunol: 68:155-159. Article link here

封面照片:肺炎链球菌 ΔlspA 菌株诱导 THP-1-Blue 细胞产生较少的 SEAP。微生物学免疫学》:68:155-159。文章链接
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引用次数: 0
Issue Information – Cover 发行信息 - 封面
IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-03-11 DOI: 10.1111/1348-0421.13125

Cover photograph: The modulatory function of circ_0008410 was examined in RASFs. The amplification of divergent primers and 518 convergent primer in cDNA and gDNA of RASFs. Microbiol Immunol: 68:100-110. Article link here

封面照片:研究了 circ_0008410 在 RASFs 中的调节功能。在 RASFs 的 cDNA 和 gDNA 中扩增分歧引物和 518 融合引物。微生物学免疫学》:68:100-110。文章链接
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引用次数: 0
Interferon inducible guanylate-binding protein 1 modulates the lipopolysaccharide-induced cytokines/chemokines and mitogen-activated protein kinases in macrophages 干扰素诱导鸟苷酸结合蛋白1可调节脂多糖诱导的细胞因子/凝血因子和巨噬细胞中的丝裂原活化蛋白激酶。
IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-03-10 DOI: 10.1111/1348-0421.13123
Ravindra Kumar, Pramod Kumar Kushawaha

Guanylate-binding proteins (GBPs) are a family of interferon (IFN)-inducible GTPases and play a pivotal role in the host immune response to microbial infections. These are upregulated in immune cells after recognizing the lipopolysaccharides (LPS), the major membrane component of Gram-negative bacteria. In the present study, the expression pattern of GBP1–7 was initially mapped in phorbol 12-myristate 13-acetate-differentiated human monocytes THP-1 and mouse macrophages RAW 264.7 cell lines stimulated with LPS. A time-dependent significant expression of GBP1–7 was observed in these cells. Moreover, among the various GBPs, GBP1 has emerged as a central player in regulating innate immunity and inflammation. Therefore, to study the specific role of GBP1 in LPS-induced inflammation, knockdown of the Gbp1 gene was carried out in both cells using small interfering RNA interference. Altered levels of different cytokines (interleukin [IL]-4, IL-10, IL-12β, IFN-γ, tumor necrosis factor-α), inducible nitric oxide synthase, histocompatibility 2, class II antigen A, protein kinase R, and chemokines (chemokine (C-X-C motif) ligand 9 [CXCL9], CXCL10, and CXCL11) in GBP1 knockdown cells were reported compared to control cells. Interestingly, the extracellular-signal-regulated kinase 1/2 mitogen-activated protein (MAP) kinases and signal transducer and activator of transcription 1 (STAT1) transcription factor levels were considerably induced in knockdown cells compared to the control cells. However, no change in the level of phosphorylated nuclear factor-kB, c-Jun, and p38 transcription factors was observed in GBP1 knockdown cells compared to the control cells. This study concludes that GBP1 may alter the expression of cytokines, chemokines, and effector molecules mediated by MAP kinases and STAT1 transcription factors.

鸟苷酸结合蛋白(GBPs)是干扰素(IFN)诱导型 GTP 酶家族的一员,在宿主对微生物感染的免疫反应中发挥着关键作用。这些蛋白在识别革兰氏阴性细菌的主要膜成分脂多糖(LPS)后在免疫细胞中上调。本研究初步绘制了 GBP1-7 在 LPS 刺激下的表达模式图,这些细胞系分别是经磷酸果胶 12 肉豆蔻酸 13 醋酸酯分化的人单核细胞 THP-1 和小鼠巨噬细胞 RAW 264.7。在这些细胞中,GBP1-7 的表达具有时间依赖性。此外,在各种 GBPs 中,GBP1 已成为调节先天免疫和炎症的核心角色。因此,为了研究 GBP1 在 LPS 诱导的炎症中的特殊作用,我们使用小干扰 RNA 干扰技术在这两种细胞中敲除了 Gbp1 基因。与对照细胞相比,GBP1 基因敲除细胞中不同细胞因子(白细胞介素 [IL]-4、IL-10、IL-12β、IFN-γ、肿瘤坏死因子-α)、诱导型一氧化氮合酶、组织相容性 2、II 类抗原 A、蛋白激酶 R 和趋化因子(趋化因子(C-X-C motif)配体 9 [CXCL9]、CXCL10 和 CXCL11)的水平均有所改变。有趣的是,与对照细胞相比,敲除细胞中的细胞外信号调节激酶 1/2丝裂原活化蛋白(MAP)激酶和信号转导及激活转录因子 1(STAT1)转录因子的水平显著提高。然而,与对照细胞相比,GBP1敲除细胞中磷酸化核因子-kB、c-Jun和p38转录因子的水平没有变化。本研究的结论是,GBP1 可能会改变由 MAP 激酶和 STAT1 转录因子介导的细胞因子、趋化因子和效应分子的表达。
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引用次数: 0
N-glycosylation of the SARS-CoV-2 spike protein at Asn331 and Asn343 is involved in spike-ACE2 binding, virus entry, and regulation of IL-6 SARS-CoV-2尖峰蛋白在Asn331和Asn343处的N-糖基化参与了尖峰蛋白与ACE2的结合、病毒的进入和IL-6的调节。
IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-03-06 DOI: 10.1111/1348-0421.13121
Tuhin Das, Shuhong Luo, Hao Tang, Jianmin Fang, Yinging Mao, Haw-Han Yen, Sabyasachi Dash, Asif Shajahan, Lauren Pepi, Steven Huang, Valerie S. Jones, Shehuo Xie, Gordon F. Huang, Jinqiao Lu, Blake Anderson, Benyue Zhang, Parastoo Azadi, Ruo-Pan Huang

The coronavirus disease 2019 (COVID-19) pandemic is an ongoing global public health crisis. The causative agent, the SARS-CoV-2 virus, enters host cells via molecular interactions between the viral spike protein and the host cell ACE2 surface protein. The SARS-CoV-2 spike protein is extensively decorated with up to 66 N-linked glycans. Glycosylation of viral proteins is known to function in immune evasion strategies but may also function in the molecular events of viral entry into host cells. Here, we show that N-glycosylation at Asn331 and Asn343 of SARS-CoV-2 spike protein is required for it to bind to ACE2 and for the entry of pseudovirus harboring the SARS-CoV-2 spike protein into cells. Interestingly, high-content glycan binding screening data have shown that N-glycosylation of Asn331 and Asn343 of the RBD is important for binding to the specific glycan molecule G4GN (Galβ−1,4 GlcNAc), which is critical for spike-RBD-ACE2 binding. Furthermore, IL-6 was identified through antibody array analysis of conditioned media of the corresponding pseudovirus assay. Mutation of N-glycosylation of Asn331 and Asn343 sites of the spike receptor-binding domain (RBD) significantly reduced the transcriptional upregulation of pro-inflammatory signaling molecule IL-6. In addition, IL-6 levels correlated with spike protein levels in COVID-19 patients' serum. These findings establish the importance of RBD glycosylation in SARS-CoV-2 pathogenesis, which can be exploited for the development of novel therapeutics for COVID-19.

2019 年冠状病毒病(COVID-19)大流行是一场持续的全球公共卫生危机。病原体 SARS-CoV-2 病毒通过病毒尖峰蛋白与宿主细胞 ACE2 表面蛋白之间的分子相互作用进入宿主细胞。SARS-CoV-2 的尖峰蛋白被多达 66 个连接的聚糖广泛修饰。已知病毒蛋白的糖基化在免疫逃避策略中起作用,但也可能在病毒进入宿主细胞的分子事件中起作用。在这里,我们发现,SARS-CoV-2尖峰蛋白的Asn331和Asn343处的N-糖基化是其与ACE2结合以及携带SARS-CoV-2尖峰蛋白的假病毒进入细胞所必需的。有趣的是,高含量糖结合筛选数据显示,RBD 的 Asn331 和 Asn343 的 N-糖基化对于与特定的糖分子 G4GN(Galβ-1,4 GlcNAc)结合非常重要,而 G4GN 对于尖峰-RBD-ACE2 的结合至关重要。此外,通过对相应假病毒试验的条件培养基进行抗体阵列分析,还鉴定出了 IL-6。穗状受体结合域(RBD)的Asn331和Asn343位点的N-糖基化突变显著降低了促炎信号分子IL-6的转录上调。此外,IL-6 的水平与 COVID-19 患者血清中穗蛋白的水平相关。这些发现证实了RBD糖基化在SARS-CoV-2发病机制中的重要性,可用于开发针对COVID-19的新型疗法。
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引用次数: 0
Establishment of COS-BK cells persistently infected with archetype BK polyomavirus 建立持续感染原型 BK 多瘤病毒的 COS-BK 细胞。
IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-03-03 DOI: 10.1111/1348-0421.13124
Souichi Nukuzuma, Hiroshi Onogi, Tetsuro Suzuki

BK polyomavirus (BKPyV) was the first human polyomavirus to be isolated from an immunosuppressed kidney transplant recipient in 1971. BKPyV reactivation causes BKPyV-associated nephropathy and hemorrhagic cystitis. However, the mechanisms underlying BKPyV replication remain unclear. In the present study, we performed the long-term cultivation of COS-7 cells transfected with archetype KOM-5 DNA, which were designated as COS-BK cells. BKPyV derived from COS-BK cells was characterized by analyzing the amount of the virus based on hemagglutination, viral replication, and the production of viral protein 1 (VP1). Immunostaining showed that VP1-positive cells accounted for a small percentage of COS-BK cells. The nucleotide sequences encompassing the origin of the DNA replication of BKPyV derived from COS-BK cells were generated from KOM-5 by the deletion of an 8-bp sequence, which did not involve T antigen binding sites. BKPyV replicated most efficiently in COS-BK cells in DMEM containing 2% fetal bovine serum. These results indicate that COS-BK cells are a suitable culture system for studying the persistent infection of archetype BKPyV.

BK 多瘤病毒(BKPyV)是 1971 年从免疫抑制肾移植受者体内分离出的第一种人类多瘤病毒。BKPyV 再活化会导致 BKPyV 相关性肾病和出血性膀胱炎。然而,BKPyV 的复制机制仍不清楚。在本研究中,我们对转染了原型 KOM-5 DNA 的 COS-7 细胞进行了长期培养,并将其命名为 COS-BK 细胞。我们根据血凝、病毒复制和病毒蛋白 1(VP1)的产生情况分析了病毒的数量,从而确定了从 COS-BK 细胞中提取的 BKPyV 的特征。免疫染色显示,VP1 阳性细胞只占 COS-BK 细胞的一小部分。从 COS-BK 细胞中提取的 BKPyV DNA 复制源的核苷酸序列是从 KOM-5 中删除 8-bp 序列后产生的,该序列不涉及 T 抗原结合位点。在含有 2% 胎牛血清的 DMEM 中,BKPyV 在 COS-BK 细胞中的复制效率最高。这些结果表明,COS-BK 细胞是研究原型 BKPyV 持续感染的合适培养系统。
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引用次数: 0
Rapid quantitative detection system for measles virus-neutralizing antibodies using HiBiT-tagged virus-like particles 使用 HiBiT 标记病毒样颗粒的麻疹病毒中和抗体快速定量检测系统。
IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-02-27 DOI: 10.1111/1348-0421.13122
Takashi Okura, Kei Miyakawa, Maino Tahara, Kenji Someya, Fumio Seki, Mayuko Nishi, Noriyuki Otsuki, Akihide Ryo

Immunological testing to detect neutralizing antibodies (NAbs) is important in measles (MV) infection control. Currently, the plaque reduction neutralization test is the only credible method for measuring actual virus NAbs; however, its feasibility is hampered by drawbacks, such as long turnaround times, low throughput, and the need for laboratory biosafety equipment. To solve these problems, we developed a simple and rapid MV-NAb detection system using lentivirus-based virus-like particles incorporated with the NanoLuc fragment peptide HiBiT comprising the MV fusion protein and hemagglutinin on their exterior surface. Overall, this simple, safe, and rapid method could be used to detect MV NAbs.

检测中和抗体(NAbs)的免疫学测试在麻疹(MV)感染控制中非常重要。目前,斑块还原中和试验是测量实际病毒 NAbs 的唯一可靠方法;然而,其可行性受到周转时间长、通量低以及需要实验室生物安全设备等缺点的阻碍。为了解决这些问题,我们开发了一种简单、快速的中病毒 NAb 检测系统,该系统使用基于慢病毒的病毒样颗粒,其外表面含有由中病毒融合蛋白和血凝素组成的 NanoLuc 片段肽 HiBiT。总之,这种简单、安全、快速的方法可用于检测中病毒 NAbs。
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引用次数: 0
MYBBP1A is required for efficient replication and gene expression of herpes simplex virus 1 单纯疱疹病毒 1 的高效复制和基因表达需要 MYBBP1A。
IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-02-24 DOI: 10.1111/1348-0421.13120
Moeka Nobe, Yuhei Maruzuru, Kosuke Takeshima, Naoto Koyanagi, Akihisa Kato, Yasushi Kawaguchi

More than 100 different herpes simplex virus 1 (HSV-1) genes belong to three major classes, and their expression is coordinately regulated and sequentially ordered in a cascade. This complex HSV-1 gene expression is thought to be regulated by various viral and host cellular proteins. A host cellular protein, Myb-binding protein 1A (MYBBP1A), has been reported to be associated with HSV-1 viral genomes in conjunction with viral and cellular proteins critical for DNA replication, repair, and transcription within infected cells. However, the role(s) of MYBBP1A in HSV-1 infections remains unclear. In this study, we examined the effects of MYBBP1A depletion on HSV-1 infection and found that MYBBP1A depletion significantly reduced HSV-1 replication, as well as the accumulation of several viral proteins. These results suggest that MYBBP1A is an important host cellular factor that contributes to HSV-1 replication, plausibly by promoting viral gene expression.

100 多种不同的单纯疱疹病毒 1(HSV-1)基因分属三大类,它们的表达受到协调调控,并按顺序排列成一个级联。这种复杂的 HSV-1 基因表达被认为受到各种病毒和宿主细胞蛋白的调控。据报道,宿主细胞蛋白--Myb 结合蛋白 1A(MYBBP1A)与 HSV-1 病毒基因组有关,与病毒和细胞蛋白一起对感染细胞内的 DNA 复制、修复和转录至关重要。然而,MYBBP1A 在 HSV-1 感染中的作用仍不清楚。在这项研究中,我们研究了 MYBBP1A 缺失对 HSV-1 感染的影响,发现 MYBBP1A 缺失能显著减少 HSV-1 复制以及几种病毒蛋白的积累。这些结果表明,MYBBP1A是一种重要的宿主细胞因子,它可能通过促进病毒基因的表达来促进HSV-1的复制。
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引用次数: 0
Current understanding of Bordetella-induced cough 目前对博德特氏菌引起的咳嗽的认识。
IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-02-06 DOI: 10.1111/1348-0421.13119
Yasuhiko Horiguchi

Typical pathogenic bacteria of the genus Bordetella cause respiratory diseases, many of which are characterized by severe coughing in host animals. In human infections with these bacteria, such as whooping cough, coughing imposes a heavy burden on patients. The pathophysiology of this severe coughing had long been uncharacterized because convenient animal models that reproduce Bordetella-induced cough have not been available. However, rat and mouse models were recently shown as useful for understanding, at least partially, the causative factors and the mechanism of Bordetella-induced cough. Many types of coughs are induced under various physiological conditions, and the neurophysiological pathways of coughing are considered to vary among animal species, including humans. However, the neurophysiological mechanisms of the coughs in different animal species have not been entirely understood, and, accordingly, the current understanding of Bordetella-induced cough is still incomplete. Nevertheless, recent research findings may open the way for the development of prophylaxis and therapeutic measures against Bordetella-induced cough.

博德特氏菌属的典型致病菌会引起呼吸道疾病,其中许多疾病的特征是宿主动物剧烈咳嗽。在人类感染这些细菌(如百日咳)时,咳嗽会给患者带来沉重的负担。长期以来,这种剧烈咳嗽的病理生理学一直没有定性,因为没有方便的动物模型来再现博德特氏菌引起的咳嗽。然而,最近的研究表明,大鼠和小鼠模型有助于了解至少部分博德特氏菌诱发咳嗽的致病因素和机制。在不同的生理条件下会诱发多种类型的咳嗽,不同动物物种(包括人类)咳嗽的神经生理途径也不尽相同。然而,不同动物物种咳嗽的神经生理机制尚未完全清楚,因此,目前对博德特氏菌诱发咳嗽的认识仍不全面。尽管如此,最近的研究成果可能为开发针对博德特氏菌引起的咳嗽的预防和治疗措施开辟了道路。
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引用次数: 0
Issue Information – Cover 发行信息 - 封面
IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-02-06 DOI: 10.1111/1348-0421.13118

Cover photograph: Distribution of predicted RpoN-regulated genes. The biological functions of 678 the genes were classified according to the database of COGs. Microbiol Immunol: 68:36-46. Article link here

封面照片:预测的 RpoN 调控基因的分布。根据 COGs 数据库对 678 个基因的生物功能进行了分类。微生物学免疫学》:68:36-46。文章链接
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引用次数: 0
Lipoprotein signal peptidase-deficient Streptococcus pneumoniae exhibits impaired Toll-like receptor 2-stimulatory activity 脂蛋白信号肽酶缺陷的肺炎链球菌表现出受损的 Toll 样受体 2 刺激活性。
IF 2.6 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-02-04 DOI: 10.1111/1348-0421.13117
Hisanori Domon, Satoru Hirayama, Toshihito Isono, Rui Saito, Katsunori Yanagihara, Yutaka Terao

Streptococcus pneumoniae is a causative agent of community-acquired pneumonia. Upon pneumococcal infection, innate immune cells recognize pneumococcal lipoproteins via Toll-like receptor 2 and induce inflammation. Here, we generated a strain of S. pneumoniae deficient in lipoprotein signal peptidase (LspA), a transmembrane type II signal peptidase required for lipoprotein maturation, to investigate the host immune response against this strain. Triton X-114 phase separation revealed that lipoprotein expression was lower in the LspA-deficient strain than in the wild-type strain. Additionally, the LspA-deficient strain decreased nuclear factor-κB activation and cytokine production in THP-1 cells, indicating impaired innate immune response against the strain.

肺炎链球菌是社区获得性肺炎的致病菌。感染肺炎球菌后,先天性免疫细胞会通过 Toll 样受体 2 识别肺炎球菌脂蛋白并诱发炎症。在这里,我们生成了一株缺乏脂蛋白信号肽酶(LspA)的肺炎球菌,以研究宿主对该菌株的免疫反应。Triton X-114 相分离显示,LspA 缺陷菌株的脂蛋白表达量低于野生型菌株。此外,LspA缺陷株降低了THP-1细胞中核因子-κB的活化和细胞因子的产生,表明针对该菌株的先天免疫反应受损。
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引用次数: 0
期刊
Microbiology and Immunology
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