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RETRACTION: Chlamydia Pneumoniae Induces Interleukin-6 and Interleukin-10 in Human Gingival Fibroblastsle.
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-04-08 DOI: 10.1111/1348-0421.13218
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引用次数: 0
Issue Information – Cover
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-04-07 DOI: 10.1111/1348-0421.13137

Cover photograph: Supersulfides play various roles in biological systems. Microbiol Immunol: 69:191-202. Article link here

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引用次数: 0
FTO Aggravates the Infiltration of Inflammatory Cells and Pulmonary Fibrosis in Silicosis Though Inducing the Imbalance of Macrophages Polarization.
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-04-01 DOI: 10.1111/1348-0421.13216
Jian-Min Fan, Xu Zhang

Silicosis is a lung disease that is very harmful. This makes the disease worse. This study looks at how the fat mass and obesity associated (FTO) gene affects macrophage M1/M2 polarisation and pulmonary fibrosis in silicosis. Macrophages were isolated from alveolar lavage fluid in silicosis and bronchiectasis (BE) patients. Gene expression was detected by reverse transcription-PCR (RT-PCR). Pulmonary fibrosis was assessed by CTFLV/TLV% using 3D CT and Masson staining assay. Enzyme-linked immunosorbent assay was applied to assess inflammatory factor level. The macrophage M1/M2 polarization characteristics (iNOS, CD206) was quantified by Immunofluorescence and Flow cytometry assays. Silicosis patients alveolar lavage macrophages polarized towards M1 type, and the expression level of M1 polarization-related chemokines also increased. More importantly, FTO gene downregulation promotes macrophage polarization to M1 type and the secretion of pro-inflammatory factor TNF-α and IL-6. And FTO knockdown can strengthen the glycolysis of macrophages, especially anaerobic glycolysis, thus inducing macrophages M1 polarization. Moreover, downregulation of FTO ameliorates silicosis pulmonary fibrosis. And FTO upregulation is associated with the M2 polarization of macrophage and the deterioration of pulmonary fibrosis in silicosis patients. FTO downregulation facilitates the infiltration of inflammatory cells by promoting M1 polarization of macrophages in silicosis.

矽肺病是一种肺部疾病,危害极大。这种情况会使病情恶化。本研究探讨了脂肪量和肥胖相关(FTO)基因如何影响矽肺病患者巨噬细胞的M1/M2极化和肺纤维化。研究人员从矽肺和支气管扩张(BE)患者的肺泡灌洗液中分离出巨噬细胞。通过反转录-PCR(RT-PCR)检测基因表达。使用三维 CT 和马森染色法通过 CTFLV/TLV% 评估肺纤维化。酶联免疫吸附试验用于评估炎症因子水平。巨噬细胞 M1/M2 极化特征(iNOS、CD206)通过免疫荧光和流式细胞计数法进行量化。结果显示,矽肺患者肺泡灌洗液巨噬细胞向 M1 型极化,与 M1 极化相关的趋化因子的表达水平也有所增加。更重要的是,FTO 基因下调可促进巨噬细胞向 M1 型极化,促进促炎因子 TNF-α 和 IL-6 的分泌。而 FTO 基因敲除可加强巨噬细胞的糖酵解,尤其是无氧糖酵解,从而诱导巨噬细胞 M1 极化。此外,下调 FTO 可改善矽肺肺纤维化。而 FTO 的上调与巨噬细胞的 M2 极化和矽肺患者肺纤维化的恶化有关。FTO 下调可促进矽肺患者巨噬细胞的 M1 极化,从而促进炎症细胞的浸润。
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引用次数: 0
RETRACTION: Expression of Small RNAs of Bordetella Pertussis Colonizing Murine Tracheas.
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-03-31 DOI: 10.1111/1348-0421.13214

Retraction: Y. Hiramatsu, K. Suzuki, D. Motooka, S. Nakamura, Y. Horiguchi, "Expression of Small RNAs of Bordetella Pertussis Colonizing Murine Tracheas," Microbiology and Immunology 64, no. 6 (2020): 469-475, https://doi.org/10.1111/1348-0421.12791. The above article, published online on 30 March, 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editors-in-Chief, Chikara Kaito, Tomoyuki Honda, and Tomohiro Sawa; the Japanese Society for Bacteriology, the Japanese Society for Virology, and the Japanese Society for Host Defense Research; and John Wiley & Sons Australia, Ltd. The retraction has been agreed due to the request from the last author and the mutual agreement among all authors, after an institutional investigation was conducted by Osaka University that recommended retraction. The institutional investigation revealed that the first author was responsible for data fabrication and falsification within Figure 1(b), Figure 1(c) and data fabrication in Figure 2 for the Bpr4, 8 panels. Therefore, the conclusions of the paper are substantially compromised.

撤回:Y. Hiramatsu, K. Suzuki, D. Motooka, S. Nakamura, Y. Horiguchi, "Expression of Small RNAs of Bordetella Pertussis Colonizing Murine Tracheas," Microbiology and Immunology 64, no. 6 (2020): 469-475, https://doi.org/10.1111/1348-0421.12791.上述文章于 2020 年 3 月 30 日在线发表于 Wiley Online Library (wileyonlinelibrary.com),经作者、期刊主编 Chikara Kaito、Tomoyuki Honda 和 Tomohiro Sawa、日本细菌学学会、日本病毒学学会和日本宿主防御研究学会以及 John Wiley & Sons Australia, Ltd.(澳大利亚约翰威利父子公司)同意,已被撤回。在大阪大学进行了机构调查并建议撤稿后,应最后一位作者的请求,经所有作者共同商定,同意撤稿。机构调查显示,第一作者对图 1(b)、图 1(c)中的数据捏造和篡改以及图 2 中 Bpr4、8 面板的数据捏造负有责任。因此,该论文的结论大打折扣。
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引用次数: 0
RETRACTION: Current Understanding of Bordetella-Induced Cough.
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-03-25 DOI: 10.1111/1348-0421.13215

Retraction: Y. Hiramatsu, "Current Understanding of Bordetella-Induced Cough," Microbiology and Immunology 68, no. 4 (2024): 123-129, https://doi.org/10.1111/1348-0421.13119. The above article, published online on 6 February, 2024 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the author; the journal Editors-in-Chief, Chikara Kaito, Tomoyuki Honda and Tomohiro Sawa; the Japanese Society for Bacteriology, the Japanese Society for Virology, and the Japanese Society for Host Defense Research; and John Wiley & Sons Australia, Ltd. The retraction has been agreed due to the author's request for retraction. After publication of this Review, some manuscripts that represent the basis for the discussion were found to be unreliable following an institutional investigation conducted by Osaka University. These manuscripts are retracted, and as a result, the conclusions of this article are considered invalid as well.

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引用次数: 0
Correction to "Bordet-Gengou Agar Medium Supplemented With Albumin-Containing Biologics for Cultivation of Bordetellae".
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-03-24 DOI: 10.1111/1348-0421.13212
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引用次数: 0
Correction to "Identification of the Minimum Region of Bordetella pertussis Vag8 Required for Interaction With C1 Inhibitor".
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-03-24 DOI: 10.1111/1348-0421.13213
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引用次数: 0
Exploring miR-577 and miR-494-3p as Emerging Biomarkers in Sepsis-Associated Acute Kidney Injury: Diagnostic and Prognostic Perspectives.
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-03-16 DOI: 10.1111/1348-0421.13210
Lixia Xu, Jingpo Li, Li Li, Qiushuang Zhang, Qiuju Feng, Lijie Bai

Sepsis-associated acute kidney injury (AKI) poses a severe threat to patients' lives and health, making early predictions, intervention, and treatment crucial. This study aims to preliminarily explore the clinical role of miR-577 and miR-494-3p in sepsis-associated AKI. The study included 70 sepsis patients with AKI, 65 sepsis patients without AKI, and a healthy control group (HC, n = 67) to set baseline miRNA levels. Urinary miR-577 and miR-494-3p levels were measured using qRT-PCR. ROC curves evaluated their diagnostic value for sepsis-associated AKI. Logistic regression analyzed AKI risk factors, while Pearson correlation explored miRNA-clinical indicator links. Cox regression models and KM curves assessed the prognostic value of miRNAs in sepsis-associated AKI patients. Sepsis-associated AKI patients showed heightened inflammatory markers, renal indicators, and APACHE II scores compared to those without AKI. However, their urinary miR-577 and miR-494-3p levels were notably lower, distinguishing them with high diagnostic value. These miRNAs inversely correlated with inflammatory markers, renal indicators, and severity scores. Logistic regression showed lactate, PCT, BUN, Scr, Cys-C, NGAL, KIM-1, and APACHE II, as risk factors, while miR-577 and miR-494-3p were protective. In deceased sepsis-associated AKI patients, these miRNAs were lower, with higher inflammatory markers, renal indicators, and severity scores. miR-577 and miR-494-3p independently predicted mortality, with lower expressions linked to higher death rates. miR-577 and miR-494-3p are closely related to sepsis-associated AKI and can serve as potential biomarkers for diagnosis and prognostic assessment.

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引用次数: 0
Classification of C-Type Lectins and Recognition of Pathogens.
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-03-12 DOI: 10.1111/1348-0421.13211
Yasunobu Miyake

C-type lectins are calcium-dependent glycan-binding proteins that play key roles in the innate immune response by recognizing pathogens. Soluble C-type lectins agglutinate and neutralize pathogens, activate the complement system, and promote pathogen clearance via opsonization. Membrane-bound C-type lectins, also known as C-type lectin receptors (CLRs), internalize pathogens and induce their degradation in lysosomes, presenting pathogen-derived antigens to MHC-II molecules to activate adaptive immunity. CLRs also have signaling capabilities. Some contain the immunoreceptor tyrosine-based activation motif (ITAM), which induces inflammatory responses by activating transcription factors, such as NF-κB and NFAT. Others contain the immunoreceptor tyrosine-based inhibitory motif (ITIM), which suppresses activating signals by activating phosphatases, such as SHP-1. This creates a balance between activation and inhibition. C-type lectins are classified into 17 groups based on their structural domains, with Groups II and V members being particularly important for pathogen recognition. In this review, we present the accumulated and recent information on pathogen recognition by C-type lectins, along with their classification and basic functions.

C 型凝集素是钙依赖性糖结合蛋白,通过识别病原体在先天性免疫反应中发挥关键作用。可溶性 C 型凝集素能凝集和中和病原体,激活补体系统,并通过疏松作用促进病原体的清除。膜结合型 C 型凝集素又称 C 型凝集素受体(CLR),可将病原体内化并诱导其在溶酶体中降解,将病原体衍生的抗原呈现给 MHC-II 分子,从而激活适应性免疫。CLRs 还具有信号传导能力。其中一些含有基于免疫受体酪氨酸的激活基序(ITAM),可通过激活转录因子(如 NF-κB 和 NFAT)诱导炎症反应。另一些则含有基于免疫受体酪氨酸的抑制基序(ITIM),通过激活磷酸酶(如 SHP-1)来抑制激活信号。这就在激活和抑制之间建立了平衡。C 型凝集素根据其结构域分为 17 类,其中第二类和第五类对病原体的识别尤为重要。在这篇综述中,我们将介绍 C 型凝集素在病原体识别方面积累的最新信息,以及它们的分类和基本功能。
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引用次数: 0
Synergistic Inactivation of Airborne Viruses by Low-Concentration Ozone With High Humidity and Temperature.
IF 1.9 4区 医学 Q4 IMMUNOLOGY Pub Date : 2025-03-11 DOI: 10.1111/1348-0421.13204
Hidekazu Nishimura, Soichiro Sakata, Isolde Dapat, Masayuki Segawa, Yuki Mizutani, Junya Imaizumi, Kazuya Shirato, Suguru Ohmiya, Masanori Katsumi, Takahiro Yokoyama

Ambient humidity, temperature, and ozone influence the viability of airborne viruses, but their synergistic effects are poorly understood, particularly regarding ozone with humidity/temperature changes. Therefore, we examined the inactivation of airborne influenza viruses and coronaviruses under combinations of low ambient ozone concentrations, relative humidity (RH) levels, and temperatures typical of daily life. Viral fluid was atomized in a closed chamber conditioned with different combinations of these factors. The atomized aerosol particles containing the virus were exposed to ambient air and then sampled for titration. Active virus levels in ambient air at 50%-85% RH with 15, 35, and 55 ppb ozone significantly decreased compared with those in ambient air with 0 ppb ozone, whereas those in ambient air at < 40% RH decreased only slightly, even with 100 ppb ozone. Viral gene copy numbers, assayed via quantitative real-time polymerase chain reaction, remained similar across all conditions. Inactivation increased with higher temperatures, although not at 15°C. These findings suggest that low concentrations of ambient ozone, when combined with high humidity and temperature, effectively inactivate airborne viruses, potentially influencing viral transmission in real-world environments.

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Microbiology and Immunology
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