Microbiology and Immunology最新文献_第3页

IF 2.6 4区医学

Microbiology and Immunology Pub Date : 2024-04-09 DOI: 10.1111/1348-0421.13126

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IF 2.6 4区医学

Microbiology and Immunology Pub Date : 2024-03-11 DOI: 10.1111/1348-0421.13125

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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

Microbiology and Immunology Pub Date : 2024-03-10 DOI: 10.1111/1348-0421.13123

Ravindra Kumar, Pramod Kumar Kushawaha

{"title":"Interferon inducible guanylate-binding protein 1 modulates the lipopolysaccharide-induced cytokines/chemokines and mitogen-activated protein kinases in macrophages","authors":"Ravindra Kumar, Pramod Kumar Kushawaha","doi":"10.1111/1348-0421.13123","DOIUrl":"10.1111/1348-0421.13123","url":null,"abstract":"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.","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140094377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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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

Microbiology and 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

{"title":"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","authors":"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","doi":"10.1111/1348-0421.13121","DOIUrl":"10.1111/1348-0421.13121","url":null,"abstract":"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.","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1348-0421.13121","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140039857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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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

Microbiology and Immunology Pub Date : 2024-03-03 DOI: 10.1111/1348-0421.13124

Souichi Nukuzuma, Hiroshi Onogi, Tetsuro Suzuki

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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

Microbiology and 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

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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

Microbiology and Immunology Pub Date : 2024-02-24 DOI: 10.1111/1348-0421.13120

Moeka Nobe, Yuhei Maruzuru, Kosuke Takeshima, Naoto Koyanagi, Akihisa Kato, Yasushi Kawaguchi

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

Microbiology and Immunology Pub Date : 2024-02-06 DOI: 10.1111/1348-0421.13119

Yasuhiko Horiguchi

{"title":"Current understanding of Bordetella-induced cough","authors":"Yasuhiko Horiguchi","doi":"10.1111/1348-0421.13119","DOIUrl":"10.1111/1348-0421.13119","url":null,"abstract":"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.","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1348-0421.13119","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139692353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Issue Information – Cover 发行信息 - 封面

IF 2.6 4区医学

Microbiology and Immunology Pub Date : 2024-02-06 DOI: 10.1111/1348-0421.13118

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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

Microbiology and Immunology Pub Date : 2024-02-04 DOI: 10.1111/1348-0421.13117

Hisanori Domon, Satoru Hirayama, Toshihito Isono, Rui Saito, Katsunori Yanagihara, Yutaka Terao

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