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Virological characteristics of the SARS-CoV-2 Omicron EG.5.1 variant SARS-CoV-2 Omicron EG.5.1 变体的病毒学特征。
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-07-04 DOI: 10.1111/1348-0421.13165
Shuhei Tsujino, Sayaka Deguchi, Tomo Nomai, Miguel Padilla-Blanco, Arnon Plianchaisuk, Lei Wang, MST Monira Begum, Keiya Uriu, Keita Mizuma, Naganori Nao, Isshu Kojima, Tomoya Tsubo, Jingshu Li, Yasufumi Matsumura, Miki Nagao, Yoshitaka Oda, Masumi Tsuda, Yuki Anraku, Shunsuke Kita, Hisano Yajima, Kaori Sasaki-Tabata, Ziyi Guo, Alfredo A. Hinay Jr., Kumiko Yoshimatsu, Yuki Yamamoto, Tetsuharu Nagamoto, Hiroyuki Asakura, Mami Nagashima, Kenji Sadamasu, Kazuhisa Yoshimura, Hesham Nasser, Michael Jonathan, Olivia Putri, Yoonjin Kim, Luo Chen, Rigel Suzuki, Tomokazu Tamura, Katsumi Maenaka, Takashi Irie, Keita Matsuno, Shinya Tanaka, Jumpei Ito, Terumasa Ikeda, Kazuo Takayama, Jiri Zahradnik, Takao Hashiguchi, Takasuke Fukuhara, Kei Sato, The Genotype to Phenotype Japan (G2P-Japan) Consortium

In middle to late 2023, a sublineage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron XBB, EG.5.1 (a progeny of XBB.1.9.2), is spreading rapidly around the world. We performed multiscale investigations, including phylogenetic analysis, epidemic dynamics modeling, infection experiments using pseudoviruses, clinical isolates, and recombinant viruses in cell cultures and experimental animals, and the use of human sera and antiviral compounds, to reveal the virological features of the newly emerging EG.5.1 variant. Our phylogenetic analysis and epidemic dynamics modeling suggested that two hallmark substitutions of EG.5.1, S:F456L and ORF9b:I5T are critical to its increased viral fitness. Experimental investigations on the growth kinetics, sensitivity to clinically available antivirals, fusogenicity, and pathogenicity of EG.5.1 suggested that the virological features of EG.5.1 are comparable to those of XBB.1.5. However, cryo-electron microscopy revealed structural differences between the spike proteins of EG.5.1 and XBB.1.5. We further assessed the impact of ORF9b:I5T on viral features, but it was almost negligible in our experimental setup. Our multiscale investigations provide knowledge for understanding the evolutionary traits of newly emerging pathogenic viruses, including EG.5.1, in the human population.

2023 年中后期,严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)的一个亚系 Omicron XBB、EG.5.1(XBB.1.9.2 的后代)正在全球迅速传播。为了揭示新出现的 EG.5.1 变体的病毒学特征,我们进行了多尺度研究,包括系统进化分析、流行动力学建模、使用假病毒、临床分离株和重组病毒在细胞培养物和实验动物中进行感染实验,以及使用人类血清和抗病毒化合物。我们的系统发育分析和流行动力学建模表明,EG.5.1的两个标志性取代,即S:F456L和ORF9b:I5T,是其提高病毒适应性的关键。对 EG.5.1 的生长动力学、对临床可用抗病毒药物的敏感性、致熔性和致病性进行的实验研究表明,EG.5.1 的病毒学特征与 XBB.1.5 相当。然而,低温电子显微镜显示 EG.5.1 和 XBB.1.5 的尖峰蛋白在结构上存在差异。我们进一步评估了 ORF9b:I5T 对病毒特征的影响,但在我们的实验装置中几乎可以忽略不计。我们的多尺度研究为了解包括EG.5.1在内的新出现的致病病毒在人类群体中的进化特征提供了知识。
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引用次数: 0
Pathogenicity of genotype 2.1 classical swine fever virus isolated from Japan in 2019 in pigs 2019 年从日本分离的基因型 2.1 经典猪瘟病毒在猪身上的致病性。
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-06-30 DOI: 10.1111/1348-0421.13160
Maiko Yamashita, Shoko Iwamoto, Mariko Ochiai, Atsushi Yamamoto, Kasumi Sudo, Rie Narushima, Takao Nagasaka, Akito Saito, Mami Oba, Tsutomu Omatsu, Tetsuya Mizutani, Kinya Yamamoto

Classical swine fever (CSF) re-emerged in Japan in 2018 for the first time in 26 years. The disease has been known to be caused by a moderately pathogenic virus, rather than the highly pathogenic virus that had occurred in the past. However, the underlying pathophysiology remains unknown. This study conducted an experimental challenge on specific pathogen-free (SPF) pigs in a naïve state for 2, 4, and 6 weeks and confirmed the disease state during each period by clinical observation, virus detection, and pathological necropsy. We revealed the pathological changes and distribution of pathogens and virus-specific antibodies at each period after virus challenge. These results were comprehensively analyzed and approximately 70% of the pigs recovered, especially at 4- and 6-week post-virus challenge. This study provides useful information for future countermeasures against CSF by clarifying the pathogenicity outcomes in unvaccinated pigs with moderately pathogenic genotype 2.1 virus.

2018 年,典型猪瘟(CSF)26 年来首次在日本再次出现。据了解,该病是由中度致病性病毒引起的,而不是过去发生的高致病性病毒。然而,其潜在的病理生理学仍然未知。本研究对无特定病原体(SPF)猪进行了为期 2 周、4 周和 6 周的试验性挑战,并通过临床观察、病毒检测和病理解剖确认了每个时期的疾病状态。我们揭示了病毒挑战后各个时期的病理变化以及病原体和病毒特异性抗体的分布情况。对这些结果进行了综合分析,约 70% 的猪只恢复了健康,尤其是在病毒挑战后 4 周和 6 周。本研究阐明了未接种疫苗的猪感染中度致病性基因型 2.1 病毒后的致病性结果,为今后采取 CSF 对策提供了有用信息。
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引用次数: 0
Tumor-associated macrophages: The key player in hepatoblastoma microenvironment and the promising therapeutic target 肿瘤相关巨噬细胞:肝母细胞瘤微环境的关键角色和有希望的治疗靶点
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-06-25 DOI: 10.1111/1348-0421.13162
Ahmad Adawy, Yoshihiro Komohara, Taizo Hibi

The tumor microenvironment of hepatoblastoma (HB), the most common pediatric liver tumor, predominantly exhibits a myeloid immune landscape. in which tumor-associated macrophages (TAMs) are considered the core component. The crosstalk between TAMs and HB cells markedly influences tumor behavior. TAM-derived factors are involved in tumor proliferation and vascular invasion. On the other hand, HB cell secretome attracts, stimulates, and reprograms TAMs to be immunosuppressive in favor of tumor invasion, rather than their innate role in combating tumor growth, such crosstalk sometimes forms bidirectional feedback loops, making the tumor more virulent and resistant to routine therapeutics. Consequently, TAMs are the common denominator of most suggested HB immunotherapeutic strategies. Macrophage immune checkpoint inhibitors, macrophage-mediated antibody-dependent cellular phagocytosis, and the novel chimeric antigen receptor macrophage therapy (CAR Mφ) are currently under trial. In this review, we will summarize the significance of TAMs and their potential role as a therapeutic target in HB.

肝母细胞瘤(HB)是最常见的小儿肝脏肿瘤,其肿瘤微环境主要表现为髓系免疫景观,其中肿瘤相关巨噬细胞(TAMs)被认为是核心组成部分。TAMs 和 HB 细胞之间的相互影响明显地影响着肿瘤的行为。TAM 衍生因子参与肿瘤增殖和血管侵袭。另一方面,HB 细胞的分泌物会吸引、刺激和重编程 TAMs,使其具有免疫抑制作用,从而有利于肿瘤的侵袭,而非其对抗肿瘤生长的固有作用,这种串扰有时会形成双向反馈回路,使肿瘤更具毒性,并对常规治疗产生抗药性。因此,TAMs 是大多数建议的 HB 免疫治疗策略的共同点。巨噬细胞免疫检查点抑制剂、巨噬细胞介导的抗体依赖性细胞吞噬作用以及新型嵌合抗原受体巨噬细胞疗法(CAR Mφ)目前正在试验中。在这篇综述中,我们将总结 TAMs 的重要性及其作为 HB 治疗靶点的潜在作用。
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引用次数: 0
A fungal-binding agglutinin in the skin slime of Japanese flounder (Paralichthys olivaceus) is glyceraldehyde 3-phosphate dehydrogenase 日本鲽(Paralichthys olivaceus)皮肤粘液中的一种真菌结合凝集素是 3-磷酸甘油醛脱氢酶。
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-06-24 DOI: 10.1111/1348-0421.13163
Shigeyuki Tsutsui, Mizuki Terashima, Osamu Nakamura

Agglutination of pathogenic microorganisms on the body surface is a significant phenomenon for the prevention of infection. In the present study, we show that an extract of the skin mucus from Japanese flounder (Paralichthys olivaceus) has agglutination activity against the yeast Saccharomyces cerevisiae. We purified this yeast-binding protein, which consists of an approximately 35-kDa homodimer, using affinity chromatography with yeast as a ligand. Multiple internal amino acid sequences of the protein, as determined using liquid chromatography with quadrupole time-of-flight tandem mass spectrometry, mapped to flounder glyceraldehyde 3-phosphate dehydrogenase (GAPDH). An anti-GAPDH antibody inhibited the yeast agglutination activity in the skin mucus extract and stained agglutinated yeast, indicating that flounder GAPDH could agglutinate yeast. The current study suggests that GAPDH, a well-known protein as the sixth enzyme in the glycolytic pathway, is a significant player in mucosal immunity in teleosts.

在体表凝集病原微生物是预防感染的一个重要现象。在本研究中,我们发现日本比目鱼(Paralichthys olivaceus)皮肤粘液提取物具有凝集酵母菌的活性。我们以酵母为配体,利用亲和层析技术纯化了这种酵母结合蛋白,它由一个约 35 kDa 的同源二聚体组成。通过液相色谱-四极杆飞行时间串联质谱测定,该蛋白的多个内部氨基酸序列与比目鱼甘油醛-3-磷酸脱氢酶(GAPDH)相对应。抗 GAPDH 抗体可抑制皮肤粘液提取物中的酵母凝集活性,并对凝集的酵母进行染色,表明比目鱼 GAPDH 可凝集酵母。本研究表明,作为糖酵解途径中第六种酶的著名蛋白质 GAPDH 在远洋鱼类的粘膜免疫中起着重要作用。
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引用次数: 0
Epigallocatechin-3-gallate ameliorates lipopolysaccharide-induced acute thymus involution in mice via AMPK/Sirt1 pathway 表没食子儿茶素-3-棓酸盐通过AMPK/Sirt1途径改善脂多糖诱导的小鼠急性胸腺萎缩。
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-06-17 DOI: 10.1111/1348-0421.13159
Qing Su, Shu-Ping Yang, Jun-Ping Guo, Yi-Ren Rong, Yun Sun, Yu-Rong Chai

The thymus, a site to culture the naïve T lymphocytes, is susceptible to atrophy or involution due to aging, inflammation, and oxidation. Epigallocatechin-3-gallate (EGCG) has been proven to possess anti-inflammatory, antioxidant, and antitumor activity. Here, we investigate the effects of EGCG on thymic involution induced by lipopolysaccharide (LPS), an endotoxin derived from Gram-negative bacteria. The methodology included an in vivo experiment on female Kunming mice exposed to LPS and EGCG. Morphological assessment of thymic involution, immunohistochemical detection, and thymocyte subsets analysis by flow cytometry were further carried out to evaluate the potential role of EGCG on the thymus. As a result, we found that EGCG alleviated LPS-induced thymic atrophy, increased mitochondrial membrane potential and superoxide dismutase levels, and decreased malondialdehyde and reactive oxygen species levels. In addition, EGCG pre-supplement restored the ratio of thymocyte subsets, the expression of autoimmune regulator, sex-determining region Y-box 2, and Nanog homebox, and reduced the number of senescent cells and collagen fiber deposition. Western blotting results indicated that EGCG treatment elevated LPS-induced decrease in pAMPK, Sirt1 protein expression. Collectively, EGCG relieved thymus architecture and function damaged by LPS via regulation of AMPK/Sirt1 signaling pathway. Our findings may provide a new strategy on protection of thymus from involution caused by LPS by using EGCG. And EGCG might be considered as a potential agent for the prevention and treatment of thymic involution.

胸腺是培养幼稚 T 淋巴细胞的场所,容易因衰老、炎症和氧化而萎缩或内陷。表没食子儿茶素-3-棓酸盐(EGCG)已被证明具有抗炎、抗氧化和抗肿瘤活性。在此,我们研究了表儿茶素-3-棓酸盐对脂多糖(LPS)(一种来自革兰氏阴性细菌的内毒素)诱导的胸腺萎缩的影响。研究方法包括对暴露于 LPS 和 EGCG 的雌性昆明小鼠进行体内实验。为了评估EGCG对胸腺的潜在作用,我们还进一步进行了胸腺萎缩的形态学评估、免疫组化检测和流式细胞术胸腺细胞亚群分析。结果发现,EGCG能缓解LPS诱导的胸腺萎缩,提高线粒体膜电位和超氧化物歧化酶水平,降低丙二醛和活性氧水平。此外,预先补充 EGCG 还能恢复胸腺细胞亚群的比例、自身免疫调节因子、性别决定区 Y-box 2 和 Nanog 同源框的表达,并减少衰老细胞的数量和胶原纤维的沉积。Western印迹检测结果表明,EGCG能提高LPS诱导的pAMPK、Sirt1蛋白表达量的下降。总之,EGCG通过调节AMPK/Sirt1信号通路,缓解了LPS对胸腺结构和功能的损伤。我们的研究结果可能为利用EGCG保护胸腺免受LPS引起的内陷提供了一种新策略。EGCG可能被认为是一种预防和治疗胸腺萎缩的潜在药物。
{"title":"Epigallocatechin-3-gallate ameliorates lipopolysaccharide-induced acute thymus involution in mice via AMPK/Sirt1 pathway","authors":"Qing Su,&nbsp;Shu-Ping Yang,&nbsp;Jun-Ping Guo,&nbsp;Yi-Ren Rong,&nbsp;Yun Sun,&nbsp;Yu-Rong Chai","doi":"10.1111/1348-0421.13159","DOIUrl":"10.1111/1348-0421.13159","url":null,"abstract":"<p>The thymus, a site to culture the naïve T lymphocytes, is susceptible to atrophy or involution due to aging, inflammation, and oxidation. Epigallocatechin-3-gallate (EGCG) has been proven to possess anti-inflammatory, antioxidant, and antitumor activity. Here, we investigate the effects of EGCG on thymic involution induced by lipopolysaccharide (LPS), an endotoxin derived from Gram-negative bacteria. The methodology included an in vivo experiment on female Kunming mice exposed to LPS and EGCG. Morphological assessment of thymic involution, immunohistochemical detection, and thymocyte subsets analysis by flow cytometry were further carried out to evaluate the potential role of EGCG on the thymus. As a result, we found that EGCG alleviated LPS-induced thymic atrophy, increased mitochondrial membrane potential and superoxide dismutase levels, and decreased malondialdehyde and reactive oxygen species levels. In addition, EGCG pre-supplement restored the ratio of thymocyte subsets, the expression of autoimmune regulator, sex-determining region Y-box 2, and Nanog homebox, and reduced the number of senescent cells and collagen fiber deposition. Western blotting results indicated that EGCG treatment elevated LPS-induced decrease in pAMPK, Sirt1 protein expression. Collectively, EGCG relieved thymus architecture and function damaged by LPS via regulation of AMPK/Sirt1 signaling pathway. Our findings may provide a new strategy on protection of thymus from involution caused by LPS by using EGCG. And EGCG might be considered as a potential agent for the prevention and treatment of thymic involution.</p>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"68 8","pages":"281-293"},"PeriodicalIF":1.9,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141419878","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}
引用次数: 0
Antibiotic susceptibility and genome analysis of Enterococcus species isolated from inpatients in one hospital with no apparent outbreak of vancomycin-resistant Enterococcus in Japan 日本一家未明显爆发耐万古霉素肠球菌疫情的医院从住院病人中分离的肠球菌的抗生素敏感性和基因组分析。
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-06-14 DOI: 10.1111/1348-0421.13155
Ayumi Fujii, Miki Kawada-Matsuo, Mi Nguyen-Tra Le, Kanako Masuda, Kayoko Tadera, Yujin Suzuki, Saki Nishihama, Junzo Hisatsune, Yo Sugawara, Seiya Kashiyama, Hideki Shiba, Tomonao Aikawa, Hiroki Ohge, Motoyuki Sugai, Hitoshi Komatsuzawa

To prevent nosocomial infection, it is important to screen for potential vancomycin-resistant Enterococcus (VRE) among patients. In this study, we analyzed enterococcal isolates from inpatients in one hospital without any apparent outbreak of VRE. Enterococcal isolates were collected from inpatients at Hiroshima University Hospital from April 1 to June 30, 2021 using selective medium for Enterococci. Multilocus sequence typing, antimicrobial susceptibility testing, and whole-genome sequencing were performed. A total of 164 isolates, including Enterococcus faecium (41 isolates), Enterococcus faecalis (80 isolates), Enterococcus raffinosus (11 isolates), Enterococcus casseliflavus (nine isolates), Enterococcus avium (12 isolates), Enterococcus lactis (eight isolates), Enterococcus gallinarum (two isolates), and Enterococcus malodoratus (one isolate), were analyzed. We found one vanA-positive E. faecium, which was already informed when the patient was transferred to the hospital, nine vanC-positive E. casseliflavus, and two vanC-positive E. gallinarum. E. faecium isolates showed resistance to ampicillin (95.1%), imipenem (95.1%), and levofloxacin (87.8%), and E. faecalis isolates showed resistance to minocycline (49.4%). Ampicillin- and levofloxacin-resistant E. faecium had multiple mutations in penicillin-binding protein 5 (PBP5) (39/39 isolates) and ParC/GyrA (21/36 isolates), respectively. E. raffinosus showed resistance to ampicillin (81.8%), imipenem (45.5%), and levofloxacin (45.5%), and E. lactis showed resistance to ampicillin (37.5%) and imipenem (50.0%). The linezolid resistance genes optrA and cfr(B) were found only in one isolate of E. faecalis and E. raffinosus, respectively. This study, showing the status of enterococci infection in hospitalized patients, is one of the important information when considering nosocomial infection control of VRE.

为预防院内感染,必须筛查患者中可能存在的耐万古霉素肠球菌(VRE)。在本研究中,我们分析了一家未明显爆发 VRE 的医院中住院患者的肠球菌分离物。我们使用肠球菌选择性培养基收集了广岛大学医院 2021 年 4 月 1 日至 6 月 30 日住院患者的肠球菌分离物。进行了多焦点序列分型、抗菌药物药敏试验和全基因组测序。共分析了 164 个分离株,包括粪肠球菌(41 个分离株)、粪肠球菌(80 个分离株)、拉菲诺斯肠球菌(11 个分离株)、卡氏肠球菌(9 个分离株)、阿维氏肠球菌(12 个分离株)、乳酸肠球菌(8 个分离株)、加里纳氏肠球菌(2 个分离株)和恶臭肠球菌(1 个分离株)。我们发现了 1 株 vanA 阳性的粪肠球菌(患者转院时已获知)、9 株 vanC 阳性的卡氏肠球菌和 2 株 vanC 阳性的加里纳氏肠球菌。分离出的粪肠球菌对氨苄西林(95.1%)、亚胺培南(95.1%)和左氧氟沙星(87.8%)具有耐药性,对米诺环素(49.4%)具有耐药性。对氨苄西林和左氧氟沙星耐药的粪肠球菌分别对青霉素结合蛋白 5(PBP5)(39/39 个分离株)和 ParC/GyrA (21/36 个分离株)有多重突变。拉菲诺斯大肠杆菌对氨苄西林(81.8%)、亚胺培南(45.5%)和左氧氟沙星(45.5%)产生耐药性,乳酸杆菌对氨苄西林(37.5%)和亚胺培南(50.0%)产生耐药性。仅在粪大肠杆菌和拉菲诺斯大肠杆菌的一个分离株中分别发现了利奈唑胺耐药基因 optrA 和 cfr(B)。这项研究显示了住院患者肠球菌感染的状况,是考虑控制 VRE 的院内感染时的重要信息之一。
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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 : 2024-06-05 DOI: 10.1111/1348-0421.13158

Cover photograph: LEfSe analysis of fecal microbiota. Microbiol Immunol: 68:206-211. Article link here

封面照片:粪便微生物群的 LEfSe 分析。微生物学免疫学》:68:206-211。文章链接
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引用次数: 0
Involvement of SARS-CoV-2 accessory proteins in immunopathogenesis SARS-CoV-2 辅助蛋白参与免疫发病机制。
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-06-04 DOI: 10.1111/1348-0421.13157
Hayato Ito, Tomokazu Tamura, Lei Wang, Kento Mori, Masumi Tsuda, Rigel Suzuki, Saori Suzuki, Kumiko Yoshimatsu, Shinya Tanaka, Takasuke Fukuhara

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the largest single-stranded RNA virus known to date. Its genome contains multiple accessory protein genes that act against host immune responses but are not required for progeny virus production. The functions of the accessory proteins in the viral life cycle have been examined, but their involvement in viral pathogenicity remains unclear. Here, we investigated the roles of the accessory proteins in viral immunopathogenicity. To this end, recombinant SARS-CoV-2 possessing nonsense mutations in the seven accessory protein open reading frames (ORFs) (ORF3a, ORF3b, ORF6, ORF7a, ORF8, ORF9b, and ORF10) was de novo generated using an early pandemic SARS-CoV-2 strain as a backbone. We confirmed that the resultant virus (termed ORF3–10 KO) did not express accessory proteins in infected cells and retained the desired mutations in the viral genome. In cell culture, the ORF3–10 KO virus exhibited similar virus growth kinetics as the parental virus. In hamsters, ORF3–10 KO virus infection resulted in mild weight loss and reduced viral replication in the oral cavity and lung tissue. ORF3–10 KO virus infection led to mild inflammation, indicating that an inability to evade innate immune sensing because of a lack of accessory proteins impairs virus growth in vivo and results in quick elimination from the body. Overall, we showed that SARS-CoV-2 accessory proteins are involved in immunopathogenicity.

严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)是迄今已知的最大的单链 RNA 病毒。它的基因组中含有多种辅助蛋白基因,这些基因能对抗宿主的免疫反应,但并不是产生后代病毒所必需的。人们已经研究了附属蛋白在病毒生命周期中的功能,但它们与病毒致病性的关系仍不清楚。在此,我们研究了附属蛋白在病毒免疫致病性中的作用。为此,我们以早期大流行的 SARS-CoV-2 株系为骨干,从头生成了在七个附属蛋白开放阅读框(ORF)(ORF3a、ORF3b、ORF6、ORF7a、ORF8、ORF9b 和 ORF10)中具有无义突变的重组 SARS-CoV-2 病毒。我们证实,产生的病毒(称为 ORF3-10 KO)在感染细胞中不表达附属蛋白,并在病毒基因组中保留了所需的突变。在细胞培养中,ORF3-10 KO 病毒表现出与亲本病毒相似的病毒生长动力学。仓鼠感染 ORF3-10 KO 病毒后体重轻微下降,口腔和肺组织中的病毒复制减少。ORF3-10 KO病毒感染会导致轻微炎症,这表明由于缺乏附属蛋白而无法躲避先天性免疫感应会影响病毒在体内的生长,并导致病毒被迅速排出体外。总之,我们发现 SARS-CoV-2 辅助蛋白参与了免疫致病性。
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引用次数: 0
Biofilm-derived membrane vesicles exhibit potent immunomodulatory activity in Pseudomonas aeruginosa PAO1 生物膜衍生的膜囊泡对铜绿假单胞菌 PAO1 表现出强大的免疫调节活性。
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-05-26 DOI: 10.1111/1348-0421.13156
Minato Takahara, Satoru Hirayama, Hiroyuki Futamata, Ryoma Nakao, Yosuke Tashiro

Pathogenic bacteria form biofilms on epithelial cells, and most bacterial biofilms show increased production of membrane vesicles (MVs), also known as outer membrane vesicles in Gram-negative bacteria. Numerous studies have investigated the MVs released under planktonic conditions; however, the impact of MVs released from biofilms on immune responses remains unclear. This study aimed to investigate the characteristics and immunomodulatory activity of MVs obtained from both planktonic and biofilm cultures of Pseudomonas aeruginosa PAO1. The innate immune responses of macrophages to planktonic-derived MVs (p-MVs) and biofilm-derived MVs (b-MVs) were investigated by measuring the mRNA expression of proinflammatory cytokines. Our results showed that b-MVs induced a higher expression of inflammatory cytokines, including Il1b, Il6, and Il12p40, than p-MVs. The mRNA expression levels of Toll-like receptor 4 (Tlr4) differed between the two types of MVs, but not Tlr2. Polymyxin B significantly neutralized b-MV-mediated cytokine induction, suggesting that lipopolysaccharide of native b-MVs is the origin of the immune response. In addition, heat-treated or homogenized b-MVs induced the mRNA expression of cytokines, including Tnfa, Il1b, Il6, and Il12p40. Heat treatment of MVs led to increased expression of Tlr2 but not Tlr4, suggesting that TLR2 ligands play a role in detecting the pathogen-associated molecular patterns in lysed MVs. Taken together, our data indicate that potent immunomodulatory MVs are produced in P. aeruginosa biofilms and that this behavior could be a strategy for the bacteria to infect host cells. Furthermore, our findings would contribute to developing novel vaccines using MVs.

致病细菌会在上皮细胞上形成生物膜,大多数细菌生物膜都会增加膜囊(MVs)的产生,革兰氏阴性细菌的膜囊也称为外膜囊。许多研究对浮游生物条件下释放的膜囊泡进行了调查,但生物膜释放的膜囊泡对免疫反应的影响仍不清楚。本研究旨在调查从铜绿假单胞菌 PAO1 的浮游生物和生物膜培养物中获得的 MVs 的特征和免疫调节活性。通过测量促炎细胞因子的 mRNA 表达,研究了巨噬细胞对浮游生物源 MVs(p-MVs)和生物膜源 MVs(b-MVs)的先天性免疫反应。结果显示,与 p-MVs 相比,b-MVs 诱导的炎性细胞因子(包括 Il1b、Il6 和 Il12p40)表达量更高。两种中毒性病毒的 Toll 样受体 4(Tlr4)的 mRNA 表达水平不同,但 Tlr2 的表达水平没有差异。多粘菌素 B 能明显中和 b-MV 介导的细胞因子诱导,这表明原生 b-MV 的脂多糖是免疫反应的起源。此外,热处理或均质化的b-MV可诱导细胞因子(包括Tnfa、Il1b、Il6和Il12p40)的mRNA表达。热处理中毒性细胞可导致 Tlr2 的表达增加,但 Tlr4 的表达却没有增加,这表明 TLR2 配体在检测裂解中毒性细胞中的病原体相关分子模式方面发挥了作用。总之,我们的数据表明,铜绿微囊藻生物膜中会产生强效的免疫调节MV,这种行为可能是细菌感染宿主细胞的一种策略。此外,我们的研究结果将有助于利用 MVs 开发新型疫苗。
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引用次数: 0
The prevention effect of Limosilactobacillus reuteri on acute kidney injury by regulating gut microbiota 通过调节肠道微生物群来预防急性肾损伤的Limosilactobacillus reuteri。
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-05-15 DOI: 10.1111/1348-0421.13130
Zhan Yang, Juan Ni, Xuewei Sun, Qian Cui, Xinrui Zhang, Mingyan Zhang, Xiaojing Zhu, Zihan Wu, Chengliang Tang, Jingfeng Zhu, Huijuan Mao, Kang Liu, Chunhui Wang, Changying Xing, Jin Zhu

Acute kidney injury (AKI) has considerably high morbidity and mortality but we do not have proper treatment for it. There is an urgent need to develop new prevention or treatment methods. Gut microbiota has a close connection with renal diseases and has become the new therapy target for AKI. In this study, we found the oral administration of the probiotic Limosilactobacillus reuteri had a prevention effect on the AKI induced by lipopolysaccharide (LPS). It reduced serum concentration of creatinine and urea nitrogen and protected the renal cells from necrosis and apoptosis. Meanwhile, L. reuteri improved the gut barrier function, which is destroyed in AKI, and modulated the gut microbiota and relevant metabolites. Compared with the LPS group, L. reuteri increased the proportion of Proteobacteria and reduced the proportion of Firmicutes, changing the overall structure of the gut microbiota. It also influenced the fecal metabolites and changed the metabolite pathways, such as tyrosine metabolism, pentose and glucuronate interconversions, galactose metabolism, purine metabolism, and insulin resistance. These results showed that L. reuteri is a potential therapy for AKI as it helps in sustaining the gut barrier integrity and modulating gut microbiota and related metabolites.

急性肾损伤(AKI)具有相当高的发病率和死亡率,但我们却没有适当的治疗方法。我们迫切需要开发新的预防或治疗方法。肠道微生物群与肾脏疾病关系密切,已成为治疗急性肾损伤的新靶点。本研究发现,口服益生菌Limosilactobacillus reuteri对脂多糖(LPS)诱导的AKI有预防作用。它能降低血清肌酐和尿素氮的浓度,保护肾细胞免受坏死和凋亡。同时,L. reuteri 还能改善 AKI 中被破坏的肠道屏障功能,调节肠道微生物群和相关代谢物。与 LPS 组相比,L. reuteri 增加了蛋白菌的比例,降低了固缩菌的比例,改变了肠道微生物群的整体结构。它还影响了粪便代谢物,改变了代谢物的途径,如酪氨酸代谢、戊糖和葡萄糖醛酸的相互转化、半乳糖代谢、嘌呤代谢和胰岛素抵抗。这些结果表明,L. reuteri 是治疗 AKI 的一种潜在疗法,因为它有助于维持肠道屏障的完整性,调节肠道微生物群和相关代谢物。
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Microbiology and Immunology
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