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Allergic Bronchopulmonary Aspergillosis (ABPA) With Colonized Aspergillus fumigatus Detected by Metagenomic Next-Generation Sequencing on Tissue Samples: A Distinct Subset of ABPA With a Higher Risk of Exacerbation 通过对组织样本进行元基因组下一代测序,检测出带有烟曲霉菌定植的过敏性支气管肺曲霉病(ABPA):具有较高恶化风险的过敏性支气管肺曲霉菌病(ABPA)的一个独特亚群。
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-06-17 DOI: 10.1111/crj.13794
Wanjun Wang, Mo Xian, Yongxia Lei, Juhua Yang, Lulu Wu
<p>To the Editor:</p><p>Allergic bronchopulmonary aspergillosis (ABPA) is an immunological pulmonary disorder caused by hypersensitivity to <i>Aspergillus</i>, which colonizes the airways of patients with asthma [<span>1</span>]. Previous studies have shown that fungal colonization in <i>Aspergillus</i>-allergic diseases could lead to more rapid airway obstruction [<span>2</span>], but they lack a direct link to clinical relevance and outcome. Therefore, we aimed to identify <i>Aspergillus fumigatus</i> colonization in ABPA patients and compare their profile without colonization.</p><p>We retrospectively analyzed the clinical data of 116 patients at the Department of Allergy and Clinical Immunology, the First Affiliated Hospital of Guangzhou Medical University, from January 2014 to October 2020, of which 96 cases were diagnosed with ABPA according to the criteria described previously [<span>3</span>]. Twenty patients with the diagnosis of refractory asthma, according to the Global Institute for Asthma (GINA), were enrolled as controls. The definition of ABPA exacerbation was worsening of clinical status, obstructive deterioration of lung function, rising total IgE levels by > 50%, and the appearance of new shallow infiltrates on radiology. All patients underwent a trans-bronchoscopy and bronchial mucosa biopsy. We utilized metagenomic next-generation sequencing for the detection of the <i>A. fumigatus</i> genome from the samples. Details about the methods are in Appendix S1.</p><p>Our study showed that the basic demographic features were similar in subjects with or without tissue colonization, except for the expectoration of mucus plugs. Eosinophil counts; blood <i>A. fumigatus</i>-sIgE, IgG, and total IgE levels; and the rate of <i>Pseudomonas aeruginosa</i> colonization were all higher in ABPA than in severe asthma. In subjects with colonization, an average of 690 ± 530 bp <i>A. fumigatus</i> nucleotide reads were detected, but only 3.9% had a positive sputum culture. The FEV<sub>1</sub>, FVC, and FEV<sub>1</sub>/FVC values were significantly lower in subjects with colonization. Higher bronchiectasis CT values (59.5 ± 7.1 vs. 34 ± 8, <i>p</i> < 0.05) and more numbers of involved lobes and segments were observed in subjects with colonization (4.8 ± 0.6 vs. 3.3 ± 1.2 and 16.2 ± 4.6 vs. 9.6 ± 4.9, both <i>p</i> < 0.05). The presence of HAM was seen in 76.4% of subjects with colonization. The duration of follow-up among the three groups was nearly identical. The ABPA subjects received a higher dosage of ICS and a longer period of oral corticosteroids. More than half of the subjects with colonization (54.9%) were treated with itraconazole. A significantly larger proportion, 24/51 (47.1% vs. 24.4%), of subjects with colonization experienced ABPA exacerbations (Table 1). Twenty-two of these 24 subjects experienced their first exacerbation after 12 months of the initial diagnosis (Appendix S2). The incidence rate of exacerbation was also signi
致编辑:过敏性支气管肺曲霉菌病(ABPA)是一种由曲霉菌过敏引起的免疫性肺部疾病,曲霉菌在哮喘患者的气道中定植[1]。先前的研究表明,曲霉菌过敏性疾病中的真菌定植可导致更快的气道阻塞[2],但这些研究缺乏与临床相关性和结果的直接联系。我们回顾性分析了广州医科大学附属第一医院过敏与临床免疫科自2014年1月至2020年10月116例患者的临床资料,其中96例根据之前描述的标准被诊断为ABPA[3]。20名根据全球哮喘研究所(GINA)诊断为难治性哮喘的患者作为对照组。ABPA 恶化的定义是临床状况恶化、肺功能阻塞性恶化、总 IgE 水平上升 50%、放射学检查出现新的浅层浸润。所有患者都接受了经支气管镜检查和支气管粘膜活检。我们利用元基因组新一代测序技术检测样本中的烟曲霉菌基因组。我们的研究表明,除排出粘液栓外,有无组织定植的受试者的基本人口学特征相似。ABPA患者的嗜酸性粒细胞计数、血液烟曲霉-SIgE、IgG和总IgE水平以及铜绿假单胞菌定植率均高于重症哮喘患者。在有定植的受试者中,平均检测到 690 ± 530 bp 的烟曲霉菌核苷酸读数,但只有 3.9% 的受试者痰培养呈阳性。定植患者的 FEV1、FVC 和 FEV1/FVC 值明显较低。定植受试者的支气管扩张 CT 值更高(59.5 ± 7.1 vs. 34 ± 8,p < 0.05),受累肺叶和肺段的数量更多(4.8 ± 0.6 vs. 3.3 ± 1.2 和 16.2 ± 4.6 vs. 9.6 ± 4.9,p < 0.05)。76.4%的定植受试者存在 HAM。三组患者的随访时间几乎相同。ABPA 受试者接受的 ICS 剂量更大,口服皮质类固醇的时间更长。超过一半的定植受试者(54.9%)接受了伊曲康唑治疗。24/51(47.1% 对 24.4%)名有定植的受试者出现了 ABPA 病情加重,这一比例明显更高(表 1)。这 24 名受试者中有 22 人在初次诊断 12 个月后首次出现病情加重(附录 S2)。有定植的受试者的病情恶化发生率也明显高于无定植的受试者(分别为每 1000 人年 216 例与 132 例;p <0.01)。与严重哮喘患者相比,ABPA 患者有更多的皮质类固醇副作用(88.2% vs. 86.7% vs. 60%,p <0.05)(表 1)。这似乎与之前的研究不一致[4]。造成这种差异的部分原因可能是元基因组测序在确定微生物群定植方面比传统方法(如痰培养或实时 PCR)具有更高的特异性[5, 6]。此外,在中国,并非所有患者都能负担伊曲康唑的费用,因此大多数患者都接受了泼尼松作为初始治疗。长期的皮质类固醇治疗会促进烟曲霉菌在下呼吸道的定植[7]。因此,在元基因组测序确认后尽快对抗原进行有针对性的干预,并进行长期抗真菌治疗,可能有利于降低未来病情恶化的风险。然而,多达 76% 的患者接受过一个疗程的抗真菌治疗,但效果不佳。开始使用奥马珠单抗(omalizumab)或甲波珠单抗(mepolizumab)治疗可能是抗真菌药物的补充治疗方案[8]。如果有效,这些生物制剂可能会对 ABPA 病情加重的住院率产生积极影响,并减少医疗支出。总之,我们的研究结果提醒临床医生根据定植状态考虑多样化的个性化治疗。
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引用次数: 0
Association between plasma proteome and pulmonary heart disease: A two-stage Mendelian randomization analysis 血浆蛋白质组与肺心病的关系:两阶段孟德尔随机分析
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-06-03 DOI: 10.1111/crj.13775
Shiyang Li, Haifeng Ding, Qi Li, Xiaobin Zeng, Yanyu Zhang, Chengyi Lai, Xiaoshuang Xie, Yongjiang Tang, Jianjun Lan

Pulmonary heart disease (PHD) involves altered structure and function of the right ventricle caused by an abnormal respiratory system that causes pulmonary hypertension. However, the association between changes in plasma proteomics and PHD remains unclear. Hence, we aimed to identify causal associations between genetically predicted plasma protein levels and PHD. Mendelian randomization was performed to test the target proteins associated with PHD. Summary statistics for the human plasma proteome and pulmonary heart disease were acquired from the UK Biobank (6038 cases and 426 977 controls) and the FinnGen study (6753 cases and 302 401 controls). Publicly available pQTLs datasets for human plasma proteins were obtained from a largescale genome-wide association study in the INTERVAL study. The results were validated using a case–control cohort. We first enrolled 3622 plasma proteins with conditionally independent genetic variants; three proteins (histo-blood group ABO system transferase, activating signal cointegration 1 complex subunit 1, and calcium/calmodulin-dependent protein kinase I [CAMK1]) were significantly associated with the risk of pulmonary heart disease in the UK Biobank cohort. Only CAMK1 was successfully replicated (odds ratio: 1.1056, 95% confidence interval: 1.019–1.095, p = 0.0029) in the FinnGen population. In addition, the level of CAMK1 in 40 patients with PHD was significantly higher (p = 0.023) than that in the control group. This work proposes that CAMK1 is associated with PHD, underscoring the importance of the calcium signaling pathway in the pathophysiology to improve therapies for PHD.

肺心病(PHD)是指呼吸系统异常导致右心室结构和功能改变,从而引起肺动脉高压。然而,血浆蛋白质组学的变化与肺心病之间的关联仍不清楚。因此,我们旨在确定基因预测的血浆蛋白水平与 PHD 之间的因果关系。我们采用孟德尔随机化方法检测了与 PHD 相关的目标蛋白质。从英国生物库(6038 例病例和 426 977 例对照)和芬兰基因研究(6753 例病例和 302 401 例对照)中获得了人类血浆蛋白质组和肺心病的汇总统计数据。人类血浆蛋白的公开 pQTLs 数据集来自 INTERVAL 研究中的大规模全基因组关联研究。研究结果通过病例对照队列进行了验证。在英国生物库队列中,有三种蛋白质(组织血型 ABO 系统转移酶、激活信号整合 1 复合亚基 1 和钙/钙调蛋白依赖性蛋白激酶 I [CAMK1])与肺心病风险显著相关。在 FinnGen 群体中,只有 CAMK1 成功地被复制(几率比:1.1056,95% 置信区间:1.019-1.095,p = 0.0029)。此外,40 名 PHD 患者的 CAMK1 水平明显高于对照组(p = 0.023)。这项研究提出,CAMK1 与 PHD 有关,强调了钙信号通路在病理生理学中的重要性,从而改进了 PHD 的疗法。
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引用次数: 0
COPD patients with high blood eosinophil counts exhibit a lower rate of omicron infection and milder post-infection symptoms 血液中嗜酸性粒细胞计数较高的慢性阻塞性肺病患者的奥米克感染率较低,感染后症状也较轻。
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-05-30 DOI: 10.1111/crj.13790
Xueli Bai, Yanan Niu, Shuang Wei, Zhifan Zhu, Min Xu, Hu Liu, Xiansheng Liu, Ruiying Wang

Background

The emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its subsequent Omicron variant has raised concerns for chronic obstructive pulmonary disease (COPD) patients due to the potential risk of disruptions to healthcare services and unknown comorbidities between COPD and Omicron.

Method

In this study, we conducted a follow-up investigation of 315 COPD patients during the Omicron outbreak at Shanxi Bethune Hospital to understand the impact of the pandemic on this vulnerable population. Among all patients, 228 were infected with Omicron, of which 82 needed hospitalizations.

Result

We found that COPD patients with high blood eosinophil (EOS) counts exhibited lower susceptibility to Omicron infection and were more likely to have milder symptoms that did not require hospitalization. Conversely, patients with low EOS counts showed higher rates of infection and hospitalization. Moreover, EOS count was positively correlated with T lymphocyte counts in hospitalized patients after Omicron infection, suggesting potential associations between EOS and specific immune responses in COPD patients during viral infections. Correlation analysis revealed a positive correlation between EOS count and lymphocyte and T-cells, and a negative correlation between EOS count and age, neutrophil, and C-reactive protein.

Conclusion

Overall, our study contributes to the knowledge of COPD management during the COVID-19 Omicron outbreak and emphasizes the importance of considering individual immune profiles to improve care for COPD patients in the face of the ongoing global health crisis.

背景:严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)及其随后的 Omicron 变体的出现引起了慢性阻塞性肺病(COPD)患者的担忧,因为这有可能导致医疗服务中断,而且慢性阻塞性肺病与 Omicron 之间存在未知的合并症:在本研究中,我们对山西白求恩医院爆发奥米克龙疫情期间的 315 名慢性阻塞性肺病患者进行了跟踪调查,以了解疫情对这一易感人群的影响。在所有患者中,有 228 人感染了 Omicron,其中 82 人需要住院治疗:我们发现,血液中嗜酸性粒细胞(EOS)计数高的慢性阻塞性肺病患者对奥米克隆感染的易感性较低,症状较轻且无需住院治疗。相反,嗜酸性粒细胞计数低的患者感染率和住院率较高。此外,在感染 Omicron 后住院的患者中,EOS 计数与 T 淋巴细胞计数呈正相关,这表明在病毒感染期间,EOS 与慢性阻塞性肺病患者的特异性免疫反应之间可能存在关联。相关分析显示,EOS计数与淋巴细胞和T细胞呈正相关,而EOS计数与年龄、中性粒细胞和C反应蛋白呈负相关:总之,我们的研究有助于了解 COVID-19 Omicron 爆发期间慢性阻塞性肺病的管理情况,并强调了在当前全球健康危机面前,考虑个体免疫特征以改善慢性阻塞性肺病患者护理的重要性。
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引用次数: 0
ZEB1-AS1 mediates bone metastasis through targeting miR-320b/BMPR1A axis in lung cancer ZEB1-AS1通过靶向miR-320b/BMPR1A轴介导肺癌骨转移
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-05-23 DOI: 10.1111/crj.13770
Nianxi Tan, Junyi Tang, Guang Chen, Weilin Jiang, Zhiqin Liu

Objective

This study aimed to explore the role and regulatory mechanism of lncRNA ZEB1-AS1 in lung cancer.

Methods

The expression of ZEB1-AS1 and miR-320b was determined by qRT-PCR. Cell viability, proliferation migration, and invasion were assessed using the CCK-8, colony-forming, and Transwell assay. EMT markers were quantified using western blot. The growth of subcutaneous tumor growth and metastatic bone tumors was evaluated in mouse model of lung cancer. Additionally, metastatic bone tumors were examined using H&E staining.

Results

ZEB1-AS1 expression was upregulated, while miR-320b levels were downregulated in lung cancer. Knockdown of ZEB1-AS1 resulted in a significant suppression of cell viability, proliferation, migration, invasion, and EMT in A549 cells. Furthermore, we confirmed the targeting relationship between ZEB1-AS1 and miR-320b, as well as between miR-320b and BMPR1A. Our findings suggested that ZEB1-AS1 regulated cell viability, proliferation, migration, and invasion, as well as EMT, in lung cancer cells by targeting the miR-320b/BMPR1A axis. Moreover, our in vivo experiments confirmed that ZEB1-AS1 mediated bone metastasis through targeting miR-320b/BMPR1A axis in mice with lung cancer.

Conclusion

ZEB1-AS1 mediated bone metastasis through targeting miR-320b/BMPR1A axis in lung cancer.

目的:探讨lncRNA ZEB1-AS1在肺癌中的作用和调控机制:本研究旨在探讨lncRNA ZEB1-AS1在肺癌中的作用及调控机制:方法:通过 qRT-PCR 检测 ZEB1-AS1 和 miR-320b 的表达。采用 CCK-8、集落形成和 Transwell 试验评估细胞活力、增殖迁移和侵袭。采用 Western 印迹法对 EMT 标记进行定量。在肺癌小鼠模型中评估了皮下肿瘤和转移性骨肿瘤的生长情况。此外,还使用 H&E 染色法检测了转移性骨肿瘤:结果:肺癌中 ZEB1-AS1 表达上调,而 miR-320b 水平下调。敲除 ZEB1-AS1 能显著抑制 A549 细胞的活力、增殖、迁移、侵袭和 EMT。此外,我们还证实了ZEB1-AS1与miR-320b以及miR-320b与BMPR1A之间的靶向关系。我们的研究结果表明,ZEB1-AS1通过靶向miR-320b/BMPR1A轴调节肺癌细胞的活力、增殖、迁移和侵袭以及EMT。此外,我们的体内实验证实,ZEB1-AS1通过靶向miR-320b/BMPR1A轴介导了肺癌小鼠的骨转移:结论:ZEB1-AS1通过靶向miR-320b/BMPR1A轴介导肺癌骨转移。
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引用次数: 0
Emerging trends in management of long COVID with a focus on pulmonary rehabilitation: A review 以肺康复为重点的长期 COVID 管理新趋势:综述。
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-05-22 DOI: 10.1111/crj.13777
Allison Y. Li, Willis X. Li, Jinghong Li

Long COVID, or post-acute sequelae of COVID-19 (PASC), represents a complex condition with persistent symptoms following SARS-Cov-2 infection. The symptoms include fatigue, dyspnoea, cognitive impairment, decreased quality of life in variable levels of severity. Potential mechanisms behind long COVID include vascular damage, immune dysregulation and viral persistence. Diagnosing long COVID involves medical evaluation by multidisciplinary team and assessment of persistent symptoms with scoring systems in development. Treatment strategies are symptom-focused, encompassing multidisciplinary care, rehabilitation and tailored exercise programmes. Pulmonary rehabilitation, an effective and critical component of long COVID management, has shown promise, particularly for patients with respiratory symptoms such as dyspnoea. These programmes, which combine exercise, breathing techniques, education and psychological support, improve symptoms, quality of life and overall recovery. Innovative technologies, such as telemedicine, wearable devices, telerehabilitation, are transforming long COVID management. Telemedicine facilitates consultations and interventions, eliminating healthcare access barriers. Wearable devices enable remote and continuous monitoring of patients during their rehabilitation activities. Telerehabilitation has proven to be safe and feasible and to have high potential for COVID-19 recovery. This review provides a concise overview of long COVID, encompassing its definition, prevalence, mechanisms, clinical manifestations, diagnosis and management approaches. It emphasizes the significance of multidisciplinary approach in diagnosis and treatment of long COVID, with focus on pulmonary rehabilitation and innovative technology advances to effectively address the management of long COVID.

长期 COVID 或 COVID-19 后遗症(PASC)是感染 SARS-Cov-2 后出现持续症状的一种复杂病症。这些症状包括疲劳、呼吸困难、认知障碍、生活质量下降等,严重程度不一。长期 COVID 的潜在机制包括血管损伤、免疫调节失调和病毒持续存在。诊断长效 COVID 需要多学科团队进行医学评估,并利用正在开发的评分系统对持续症状进行评估。治疗策略以症状为中心,包括多学科护理、康复和量身定制的运动计划。肺康复是长期慢性阻塞性肺气肿治疗的一个有效且关键的组成部分,尤其是对有呼吸困难等呼吸道症状的患者而言,已显示出良好的前景。这些计划结合了运动、呼吸技巧、教育和心理支持,可改善症状、生活质量和整体康复。远程医疗、可穿戴设备、远程康复等创新技术正在改变长期的 COVID 管理。远程医疗为咨询和干预提供了便利,消除了获得医疗服务的障碍。可穿戴设备可在患者康复活动期间对其进行远程和持续监测。远程康复已被证明是安全可行的,并具有促进 COVID-19 康复的巨大潜力。本综述简明扼要地概述了长期 COVID,包括其定义、发病率、机制、临床表现、诊断和管理方法。它强调了多学科方法在诊断和治疗长COVID中的重要意义,重点关注肺康复和创新技术的发展,以有效解决长COVID的管理问题。
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引用次数: 0
Exogenous surfactant for lung contusion causing ARDS: A systematic review of clinical and experimental reports 外源性表面活性物质治疗导致 ARDS 的肺挫伤:临床和实验报告的系统回顾。
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-05-22 DOI: 10.1111/crj.13776
Tomáš Merkl, David Astapenko, Radek Štichhauer, Antonín Šafus, Tomáš Dušek, Jiří Kotek, David Řehák, Petr Lochman

This systematic review aimed to summarize the available data on the treatment of pulmonary contusions with exogenous surfactants, determine whether this treatment benefits patients with severe pulmonary contusions, and evaluate the optimal type of surfactant, method of administration, and drug concentration. Three databases (MEDline, Scopus, and Web of Science) were searched using the following keywords: pulmonary surfactant, surface-active agents, exogenous surfactant, pulmonary contusion, and lung contusion for articles published between 1945 and February 2023, with no language restrictions. Four reviewers independently rated the studies for inclusion, and the other four reviewers resolved conflicts. Of the 100 articles screened, six articles were included in the review. Owing to the limited number of papers on this topic, various types of studies were included (two clinical studies, two experiments, and two case reports). In all the studies, surfactant administration improved the selected ventilation parameters. The most frequently used type of surfactant was Curosurf® in the concentration of 25 mg/kg of ideal body weight. In most studies, the administration of a surfactant by bronchoscopy into the segmental bronchi was the preferable way of administration. In both clinical studies, patients who received surfactants required shorter ventilation times. The administration of exogenous surfactants improved ventilatory parameters and, thus, reduced the need for less aggressive artificial lung ventilation and ventilation days. The animal-derived surfactant Curosurf® seems to be the most suitable substance; however, the ideal concentration remains unclear. The ideal route of administration involves a bronchoscope in the segmental bronchi.

本系统性综述旨在总结使用外源性表面活性物质治疗肺挫伤的现有数据,确定这种治疗方法是否对严重肺挫伤患者有益,并评估最佳的表面活性物质类型、给药方法和药物浓度。使用以下关键词在三个数据库(MEDline、Scopus 和 Web of Science)中检索了 1945 年至 2023 年 2 月间发表的文章:肺表面活性物质、表面活性剂、外源性表面活性物质、肺挫伤和肺挫伤,语言不限。四位审稿人对纳入的研究进行了独立评分,其他四位审稿人解决了冲突问题。在筛选出的 100 篇文章中,有 6 篇被纳入综述。由于该主题的论文数量有限,因此纳入了各种类型的研究(两项临床研究、两项实验和两项病例报告)。在所有研究中,表面活性物质的使用都改善了所选的通气参数。最常用的表面活性剂是 Curosurf®,浓度为 25 毫克/千克理想体重。在大多数研究中,通过支气管镜将表面活性物质注入节段性支气管是较好的给药方式。在两项临床研究中,接受表面活性物质治疗的患者所需的通气时间更短。外源性表面活性物质的应用改善了通气参数,从而减少了对低强度人工肺通气和通气天数的需求。动物源性表面活性物质 Curosurf® 似乎是最合适的物质,但理想的浓度仍不明确。理想的给药途径是在节段性支气管内使用支气管镜。
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引用次数: 0
Identification and analysis of prognostic immune cell homeostasis characteristics in lung adenocarcinoma 肺腺癌预后免疫细胞稳态特征的识别与分析
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-05-17 DOI: 10.1111/crj.13755
Yidan Sun, Qianqian Ma, Yixun Chen, Dongying Liao, Fanming Kong

Background

Lung adenocarcinoma (LUAD) is one of the most invasive malignant tumor of the respiratory system. It is also the common pathological type leading to the death of LUAD. Maintaining the homeostasis of immune cells is an important way for anti-tumor immunotherapy. However, the biological significance of maintaining immune homeostasis and immune therapeutic effect has not been well studied.

Methods

We constructed a diagnostic and prognostic model for LUAD based on B and T cells homeostasis-related genes. Minimum absolute contraction and selection operator (LASSO) analysis and multivariate Cox regression are used to identify the prognostic gene signatures. Based on the overall survival time and survival status of LUAD patients, a 10-gene prognostic model composed of ABL1, BAK1, IKBKB, PPP2R3C, CCNB2, CORO1A, FADD, P2RX7, TNFSF14, and ZC3H8 was subsequently identified as prognostic markers from The Cancer Genome Atlas (TCGA)-LUAD to develop a prognostic signature. This study constructed a gene prognosis model based on gene expression profiles and corresponding survival information through survival analysis, as well as 1-year, 3-year, and 5-year ROC curve analysis. Enrichment analysis attempted to reveal the potential mechanism of action and molecular pathway of prognostic genes. The CIBERSORT algorithm calculated the infiltration degree of 22 immune cells in each sample and compared the difference of immune cell infiltration between high-risk group and low-risk group. At the cellular level, PCR and CKK8 experiments were used to verify the differences in the expression of the constructed 10-gene model and its effects on cell viability, respectively. The experimental results supported the significant biological significance and potential application value of the molecular model in the prognosis of lung cancer. Enrichment analyses showed that these genes were mainly related to lymphocyte homeostasis.

Conclusion

We identified a novel immune cell homeostasis prognostic signature. Targeting these immune cell homeostasis prognostic genes may be an alternative for LUAD treatment. The reliability of the prediction model was confirmed at bioinformatics level, cellular level, and gene level.

背景 肺腺癌(LUAD)是呼吸系统中侵袭性最强的恶性肿瘤之一。它也是导致肺腺癌患者死亡的常见病理类型。维持免疫细胞的平衡是抗肿瘤免疫疗法的重要途径。然而,维持免疫平衡的生物学意义和免疫治疗效果尚未得到很好的研究。 方法 我们根据 B 细胞和 T 细胞平衡相关基因构建了一个 LUAD 诊断和预后模型。采用最小绝对收缩和选择算子(LASSO)分析和多变量 Cox 回归确定预后基因特征。根据LUAD患者的总生存时间和生存状态,随后从The Cancer Genome Atlas (TCGA)-LUAD中确定了由ABL1、BAK1、IKBKB、PPP2R3C、CCNB2、CORO1A、FADD、P2RX7、TNFSF14和ZC3H8组成的10个基因预后模型作为预后标志物,从而建立了预后特征。本研究根据基因表达谱构建了基因预后模型,并通过生存分析以及1年、3年和5年ROC曲线分析获得了相应的生存信息。富集分析试图揭示预后基因的潜在作用机制和分子途径。CIBERSORT 算法计算了每个样本中 22 个免疫细胞的浸润程度,并比较了高危组和低危组免疫细胞浸润的差异。在细胞层面,利用 PCR 和 CKK8 实验分别验证了所构建的 10 基因模型的表达差异及其对细胞活力的影响。实验结果支持了该分子模型在肺癌预后中的重要生物学意义和潜在应用价值。富集分析表明,这些基因主要与淋巴细胞稳态有关。 结论 我们发现了一种新的免疫细胞稳态预后特征。以这些免疫细胞平衡预后基因为靶点可能是治疗肺癌的一种选择。预测模型的可靠性在生物信息学水平、细胞水平和基因水平上都得到了证实。
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引用次数: 0
CircST6GAL1 knockdown alleviates pulmonary arterial hypertension by regulating miR-509-5p/multiple C2 and transmembrane domain containing 2 axis CircST6GAL1敲除可通过调节miR-509-5p/多C2和含跨膜域2轴缓解肺动脉高压。
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-05-15 DOI: 10.1111/crj.13771
Xing Zhang, Hao Qin, Qiang Ma, Junbo Zhang, Hongyan Tian, Yan Meng

Background

Hypertension is a main contributing factor of cardiovascular diseases; deregulated circular RNAs are involved in the pathogenesis of pulmonary arterial hypertension (PAH). Herein, we evaluated the function and mechanism of circST6GAL1 in PAH process.

Methods

Human pulmonary artery smooth muscle cells (HPASMCs) were cultured in hypoxic environment for functional analysis. The cell counting kit-8, 5-ethynyl-2′-deoxyuridine, wound healing, and flow cytometry assays were used to investigate cell proliferation, migration, and apoptosis. qRT-PCR and Western blotting analyses were used for level measurement of genes and proteins. The binding between miR-509-5p and circST6GAL1 or multiple C2 and transmembrane domain containing 2 (MCTP2) was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and pull-down assays. The monocrotaline (MCT)-induced PAH mouse models were established for in vivo assay.

Results

CircST6GAL1 was highly expressed in PAH patients and hypoxia-induced HPASMCs. Functionally, circST6GAL1 deficiency reversed hypoxia-induced proliferation and migration, as well as apoptosis arrest in HPASMCs. Mechanistically, circST6GAL1 directly targeted miR-509-5p, and MCTP2 was a target of miR-509-5p. Rescue assays showed that the regulatory effects of circST6GAL1 deficiency on hypoxia-induced HPASMCs were abolished. Moreover, forced expression of miR-509-5p suppressed HPASMC proliferation and migration and induced cell apoptosis under hypoxia stimulation, while these effects were abolished by MCTP2 overexpression. Moreover, circST6GAL1 silencing improved MCT-induced pulmonary vascular remodeling and PAH.

Conclusion

CircST6GAL1 deficiency reversed hypoxia-induced proliferation and migration, as well as apoptosis arrest in HPASMCs, and alleviated pulmonary vascular remodeling in MCT-induced PAH mouse models through the miR-509-5p/MCTP2 axis, indicating a potential therapeutic target for PAH.

背景:高血压是心血管疾病的主要诱因之一,而环状 RNA 的失调与肺动脉高压(PAH)的发病机制有关。方法:在缺氧环境下培养人肺动脉平滑肌细胞(HPASMCs)进行功能分析。采用细胞计数试剂盒-8、5-乙炔基-2'-脱氧尿苷、伤口愈合和流式细胞术检测细胞的增殖、迁移和凋亡。通过双荧光素酶报告、RNA 免疫沉淀和牵引试验分析了 miR-509-5p 与 circST6GAL1 或含有多个 C2 和跨膜结构域的 2(MCTP2)之间的结合。建立了单克隆(MCT)诱导的 PAH 小鼠模型,用于体内检测:结果:CircST6GAL1在PAH患者和缺氧诱导的HPASMCs中高表达。从功能上讲,circST6GAL1的缺乏可逆转缺氧诱导的HPASMCs的增殖和迁移以及凋亡抑制。从机理上讲,circST6GAL1直接靶向miR-509-5p,而MCTP2是miR-509-5p的靶标。拯救实验表明,circST6GAL1缺乏对缺氧诱导的HPASMCs的调控作用被取消。此外,在缺氧刺激下,强制表达 miR-509-5p 可抑制 HPASMC 的增殖和迁移,并诱导细胞凋亡,而过表达 MCTP2 则可消除这些效应。此外,沉默circST6GAL1可改善MCT诱导的肺血管重塑和PAH:结论:CircST6GAL1的缺失通过miR-509-5p/MCTP2轴逆转了缺氧诱导的HPASMCs的增殖和迁移以及凋亡停滞,并缓解了MCT诱导的PAH小鼠模型的肺血管重塑,这表明CircST6GAL1是PAH的潜在治疗靶点。
{"title":"CircST6GAL1 knockdown alleviates pulmonary arterial hypertension by regulating miR-509-5p/multiple C2 and transmembrane domain containing 2 axis","authors":"Xing Zhang,&nbsp;Hao Qin,&nbsp;Qiang Ma,&nbsp;Junbo Zhang,&nbsp;Hongyan Tian,&nbsp;Yan Meng","doi":"10.1111/crj.13771","DOIUrl":"10.1111/crj.13771","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Hypertension is a main contributing factor of cardiovascular diseases; deregulated circular RNAs are involved in the pathogenesis of pulmonary arterial hypertension (PAH). Herein, we evaluated the function and mechanism of circST6GAL1 in PAH process.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Human pulmonary artery smooth muscle cells (HPASMCs) were cultured in hypoxic environment for functional analysis. The cell counting kit-8, 5-ethynyl-2′-deoxyuridine, wound healing, and flow cytometry assays were used to investigate cell proliferation, migration, and apoptosis. qRT-PCR and Western blotting analyses were used for level measurement of genes and proteins. The binding between miR-509-5p and circST6GAL1 or multiple C2 and transmembrane domain containing 2 (MCTP2) was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and pull-down assays. The monocrotaline (MCT)-induced PAH mouse models were established for in vivo assay.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CircST6GAL1 was highly expressed in PAH patients and hypoxia-induced HPASMCs. Functionally, circST6GAL1 deficiency reversed hypoxia-induced proliferation and migration, as well as apoptosis arrest in HPASMCs. Mechanistically, circST6GAL1 directly targeted miR-509-5p, and MCTP2 was a target of miR-509-5p. Rescue assays showed that the regulatory effects of circST6GAL1 deficiency on hypoxia-induced HPASMCs were abolished. Moreover, forced expression of miR-509-5p suppressed HPASMC proliferation and migration and induced cell apoptosis under hypoxia stimulation, while these effects were abolished by MCTP2 overexpression. Moreover, circST6GAL1 silencing improved MCT-induced pulmonary vascular remodeling and PAH.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>CircST6GAL1 deficiency reversed hypoxia-induced proliferation and migration, as well as apoptosis arrest in HPASMCs, and alleviated pulmonary vascular remodeling in MCT-induced PAH mouse models through the miR-509-5p/MCTP2 axis, indicating a potential therapeutic target for PAH.</p>\u0000 </section>\u0000 </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"18 5","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.13771","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140923905","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}
引用次数: 0
Human epididymis protein 4, a novel potential biomarker for diagnostic and prognosis monitoring of lung cancer 人类附睾蛋白 4--用于肺癌诊断和预后监测的新型潜在生物标记物
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-05-14 DOI: 10.1111/crj.13774
Tingting Zhang, Lanhe Chu, Wenchong Tan, Cuiping Ye, Hangming Dong

Objective

This study aimed to explore the application value of human epididymis protein 4 (HE4) in diagnosing and monitoring the prognosis of lung cancer.

Methods

First, TCGA (The Cancer Genome Atlas) databases were used to analyze whey-acidic-protein 4-disulfide bond core domain 2 (WFDC2) gene expression levels in lung cancer tissues. Then, a total of 160 individuals were enrolled, categorized into three groups: the lung cancer group (n = 80), the benign lesions group (n = 40), and the healthy controls group (n = 40). Serum HE4 levels and other biomarkers were quantified using an electro-chemiluminescent immunoassay. Additionally, the expression of HE4 in tissues was analyzed through immunohistochemistry (IHC). In vitro cultures of human airway epithelial (human bronchial epithelial [HBE]) cells and various lung cancer cell lines (SPC/PC9/A594/H520) were utilized to detect HE4 levels via western blot (WB).

Results

Analysis of the TCGA and UALCAN (The University of Alabama at Birmingham Cancer Data Analysis Portal) databases showed that WFDC2 gene expression levels were upregulated in lung cancer tissues (p < 0.01). Compared with the control group and the benign group, HE4 was significantly higher in the serum of patients with lung cancer (p < 0.001). Receiver operating characteristic (ROC) analysis confirmed that HE4 had better diagnostic efficacy than classical markers in the differential diagnosis of lung cancer and benign lesions and had the highest diagnostic value in lung adenocarcinoma (area under the ROC curve [AUC] = 0.826). HE4 increased in early lung cancer and positively correlated with poor prognosis (p < 0.001). Moreover, the results of WB and IHC revealed that the expression of HE4 was increased in lung cancer cells (SPC/A549/H520) and lung cancer tissues but decreased in PC9 cells with a lack of exon EGFR19 (p < 0.05).

Conclusion

Serum HE4 emerges as a promising novel biomarker for the diagnosis and prognosis assessment of lung cancer.

目的:探讨人附睾蛋白4(HE4)在诊断和监测肺癌预后中的应用价值:本研究旨在探讨人附睾蛋白4(HE4)在肺癌诊断和预后监测中的应用价值:首先,利用TCGA(The Cancer Genome Atlas)数据库分析肺癌组织中乳清酸性蛋白4-二硫键核心域2(WFDC2)的基因表达水平。随后,研究人员共招募了 160 人,分为三组:肺癌组(80 人)、良性病变组(40 人)和健康对照组(40 人)。采用电化学发光免疫测定法对血清 HE4 水平和其他生物标志物进行量化。此外,还通过免疫组织化学(IHC)分析了组织中 HE4 的表达。体外培养人气道上皮细胞(人支气管上皮细胞 [HBE])和各种肺癌细胞系(SPC/PC9/A594/H520),通过免疫印迹(WB)检测 HE4 的水平:结果:对TCGA和UALCAN(阿拉巴马大学伯明翰分校癌症数据分析门户网站)数据库的分析表明,WFDC2基因表达水平在肺癌组织中上调(p 结论:血清HE4是肺癌的一个重要靶标:血清 HE4 是一种很有前景的新型生物标记物,可用于肺癌的诊断和预后评估。
{"title":"Human epididymis protein 4, a novel potential biomarker for diagnostic and prognosis monitoring of lung cancer","authors":"Tingting Zhang,&nbsp;Lanhe Chu,&nbsp;Wenchong Tan,&nbsp;Cuiping Ye,&nbsp;Hangming Dong","doi":"10.1111/crj.13774","DOIUrl":"10.1111/crj.13774","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aimed to explore the application value of human epididymis protein 4 (HE4) in diagnosing and monitoring the prognosis of lung cancer.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>First, TCGA (The Cancer Genome Atlas) databases were used to analyze whey-acidic-protein 4-disulfide bond core domain 2 (WFDC2) gene expression levels in lung cancer tissues. Then, a total of 160 individuals were enrolled, categorized into three groups: the lung cancer group (<i>n</i> = 80), the benign lesions group (<i>n</i> = 40), and the healthy controls group (<i>n</i> = 40). Serum HE4 levels and other biomarkers were quantified using an electro-chemiluminescent immunoassay. Additionally, the expression of HE4 in tissues was analyzed through immunohistochemistry (IHC). In vitro cultures of human airway epithelial (human bronchial epithelial [HBE]) cells and various lung cancer cell lines (SPC/PC9/A594/H520) were utilized to detect HE4 levels via western blot (WB).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Analysis of the TCGA and UALCAN (The University of Alabama at Birmingham Cancer Data Analysis Portal) databases showed that WFDC2 gene expression levels were upregulated in lung cancer tissues (<i>p</i> &lt; 0.01). Compared with the control group and the benign group, HE4 was significantly higher in the serum of patients with lung cancer (<i>p</i> &lt; 0.001). Receiver operating characteristic (ROC) analysis confirmed that HE4 had better diagnostic efficacy than classical markers in the differential diagnosis of lung cancer and benign lesions and had the highest diagnostic value in lung adenocarcinoma (area under the ROC curve [AUC] = 0.826). HE4 increased in early lung cancer and positively correlated with poor prognosis (<i>p</i> &lt; 0.001). Moreover, the results of WB and IHC revealed that the expression of HE4 was increased in lung cancer cells (SPC/A549/H520) and lung cancer tissues but decreased in PC9 cells with a lack of exon EGFR19 (<i>p</i> &lt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Serum HE4 emerges as a promising novel biomarker for the diagnosis and prognosis assessment of lung cancer.</p>\u0000 </section>\u0000 </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"18 5","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.13774","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140917658","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}
引用次数: 0
Establishment and validation of multiclassification prediction models for pulmonary nodules based on machine learning 基于机器学习的肺结节多分类预测模型的建立和验证。
IF 1.7 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-05-12 DOI: 10.1111/crj.13769
Qiao Liu, Xue Lv, Daiquan Zhou, Na Yu, Yuqin Hong, Yan Zeng

Background

Lung cancer is the leading cause of cancer-related death worldwide. This study aimed to establish novel multiclassification prediction models based on machine learning (ML) to predict the probability of malignancy in pulmonary nodules (PNs) and to compare with three published models.

Methods

Nine hundred fourteen patients with PNs were collected from four medical institutions (A, B, C and D), which were organized into tables containing clinical features, radiologic features and laboratory test features. Patients were divided into benign lesion (BL), precursor lesion (PL) and malignant lesion (ML) groups according to pathological diagnosis. Approximately 80% of patients in A (total/male: 632/269, age: 57.73 ± 11.06) were randomly selected as a training set; the remaining 20% were used as an internal test set; and the patients in B (total/male: 94/53, age: 60.04 ± 11.22), C (total/male: 94/47, age: 59.30 ± 9.86) and D (total/male: 94/61, age: 62.0 ± 11.09) were used as an external validation set. Logical regression (LR), decision tree (DT), random forest (RF) and support vector machine (SVM) were used to establish prediction models. Finally, the Mayo model, Peking University People's Hospital (PKUPH) model and Brock model were externally validated in our patients.

Results

The AUC values of RF model for MLs, PLs and BLs were 0.80 (95% CI: 0.73–0.88), 0.90 (95% CI: 0.82–0.99) and 0.75 (95% CI: 0.67–0.88), respectively. The weighted average AUC value of the RF model for the external validation set was 0.71 (95% CI: 0.67–0.73), and its AUC values for MLs, PLs and BLs were 0.71 (95% CI: 0.68–0.79), 0.98 (95% CI: 0.88–1.07) and 0.68 (95% CI: 0.61–0.74), respectively. The AUC values of the Mayo model, PKUPH model and Brock model were 0.68 (95% CI: 0.62–0.74), 0.64 (95% CI: 0.58–0.70) and 0.57 (95% CI: 0.49–0.65), respectively.

Conclusions

The RF model performed best, and its predictive performance was better than that of the three published models, which may provide a new noninvasive method for the risk assessment of PNs.

背景:肺癌是全球癌症相关死亡的主要原因。本研究旨在建立基于机器学习(ML)的新型多分类预测模型,以预测肺结节(PNs)的恶性概率,并与已发表的三种模型进行比较:从四家医疗机构(A、B、C 和 D)收集了 914 名肺结节患者,并将其整理成包含临床特征、放射学特征和实验室检查特征的表格。根据病理诊断将患者分为良性病变组(BL)、前驱病变组(PL)和恶性病变组(ML)。随机抽取 A 组(总人数/男性:632/269,年龄:57.73±11.06)约 80% 的患者作为训练集,其余 20% 的患者作为内部测试集,B 组(总人数/男性:94/53,年龄:60.04±11.22)、C 组(总人数/男性:94/47,年龄:59.30±9.86)和 D 组(总人数/男性:94/61,年龄:62.0±11.09)的患者作为外部验证集。使用逻辑回归(LR)、决策树(DT)、随机森林(RF)和支持向量机(SVM)建立预测模型。最后,梅奥模型、北京大学人民医院(PKUPH)模型和布洛克模型在本院患者中进行了外部验证:RF模型对MLs、PLs和BLs的AUC值分别为0.80(95% CI:0.73-0.88)、0.90(95% CI:0.82-0.99)和0.75(95% CI:0.67-0.88)。外部验证集的 RF 模型加权平均 AUC 值为 0.71(95% CI:0.67-0.73),ML、PL 和 BL 的 AUC 值分别为 0.71(95% CI:0.68-0.79)、0.98(95% CI:0.88-1.07)和 0.68(95% CI:0.61-0.74)。梅奥模型、PKUPH 模型和布洛克模型的 AUC 值分别为 0.68(95% CI:0.62-0.74)、0.64(95% CI:0.58-0.70)和 0.57(95% CI:0.49-0.65):射频模型表现最佳,其预测性能优于已发表的三种模型,可为 PN 风险评估提供一种新的无创方法。
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引用次数: 0
期刊
Clinical Respiratory Journal
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