Eosinophil

嗜酸性粒细胞
  • 文章类型: Case Reports
    我们报告了使用贝那利珠单抗治疗的12岁以下儿童的首例嗜酸性粒细胞性胃炎(EoG)。在7年,我们的患者在对高剂量奥美拉唑的各种组合无效后开始服用贝那利珠单抗,消除牛奶的饮食,口腔粘稠布地奈德,口服全身性类固醇.他的胃肠道组织嗜酸性粒细胞完全耗尽,症状得到改善,但随着背景治疗的逐渐减少,症状性发作。然而,服用benralizumab4年后,他再次出现症状.Benralizumab可能是对全身性类固醇难治性EoG的可行选择,但仅作为短期辅助治疗。需要更可靠的长期数据研究,尤其是在这个年轻的人群中。
    We report one of the first cases of eosinophilic gastritis (EoG) in a child under 12 years treated with benralizumab. At 7 years, our patient was started on benralizumab after failing to respond to various combinations of high-dose omeprazole, milk elimination diet, oral viscous budesonide, and oral systemic steroids. He had a complete depletion of gastrointestinal tissue eosinophils with improved symptoms but had symptomatic flares with tapering of background therapy. However, after 4 years on benralizumab he became symptomatic again. Benralizumab may be a viable option for EoG refractory to systemic steroids but only as a short-term adjunct therapy. More robust studies with long-term data are needed, especially in this younger population.
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  • 文章类型: Journal Article
    背景和目的在全球范围内,中风是导致残疾和死亡率的主要因素之一。缺血性卒中病理生理学的最新进展强调了免疫系统在卒中相关损伤和神经保护中的重要作用。本文研究了血红蛋白水平与白细胞计数之间的关系。材料与方法2019年1月1日至2022年4月1日,纳入所有在KanuniSultanSüleyman训练研究医院急诊科确诊为急性缺血性卒中并在卒中发病4.5小时内接受静脉注射重组组织型纤溶酶原激活剂(r-tPA)治疗的18岁及以上患者。性别,年龄,出现症状,投诉,美国国立卫生研究院卒中量表(NIHSS)评分,中风影响区域,以及白细胞,中性粒细胞,血小板,嗜酸性粒细胞,淋巴细胞,记录和血红蛋白水平,并在死亡率和幸存者组之间进行比较.结果共61人,包括33名男性和28名女性,包括在研究中。随访期间死亡4例。入院时症状的平均持续时间为86.23±56.37分钟。患者的平均NIHSS评分为9.16±3.88(最小:4,最大:18)。年龄和症状持续时间之间存在统计学上显著的正相关(p<0.002,r:0.391)。嗜酸性粒细胞计数与NIHSS评分(p<0.012,r:-0.321)之间以及嗜酸性粒细胞计数与症状持续时间(p<0.042,r:-0.261)之间存在统计学上的显着负相关。血红蛋白水平与死亡率呈负相关(p<0.013,r:-0.318)。嗜酸性粒细胞与中性粒细胞比率(ENR)与NIHSS评分(p<0.017,r:-0.305)之间以及ENR与症状持续时间(p<0.034,r:-0.271)之间观察到统计学上显着的负相关。在逻辑回归模型中,血红蛋白是死亡率的重要预测因子(p<0.05,CI:0.253-0.942)。血红蛋白每增加一个单位,死亡率降低了0.488倍.结论某些血细胞类型(中性粒细胞,嗜酸性粒细胞,和淋巴细胞)在确定中风预后中起积极作用。对白细胞类型的作用的详细解释为“免疫调节”奠定了基础,“这可能是未来中风患者的一种有希望的新型治疗方式。
    Background and aim Stroke ranks among the primary contributors to disability and mortality on a global scale. Recent advances in ischemic stroke pathophysiology emphasize the significant role of the immune system in both stroke-related damage and neuroprotection. This article investigates the relationship between hemoglobin level and white blood cell count. Materials and methods From January 1, 2019, to April 1, 2022, all patients aged 18 years and over who were diagnosed with acute ischemic stroke in the emergency department of Kanuni Sultan Süleyman Training and Research Hospital and treated with intravenous recombinant tissue plasminogen activator (r-tPA) within 4.5 hours of stroke onset were included in this cross-sectional retrospective study. Gender, age, onset of symptoms, complaints, National Institutes of Health Stroke Scale (NIHSS) score, stroke-affected area, as well as leukocyte, neutrophil, platelet, eosinophil, lymphocyte, and hemoglobin levels were recorded and compared between mortality and survivor groups. Results A total of 61 people, including 33 men and 28 women, were included in the study. Four patients died during follow-ups. The mean duration of symptoms upon admission was 86.23 ± 56.37 minutes. The mean NIHSS score of patients was found to be 9.16 ± 3.88 (minimum: 4, maximum: 18). There was a statistically significant positive correlation between age and symptom duration (p < 0.002, r: 0.391). A statistically significant negative correlation was found between eosinophil count and NIHSS score (p < 0.012, r: -0.321) and between eosinophil count and symptom duration (p < 0.042, r: -0.261). There was a negative correlation between hemoglobin levels and mortality (p < 0.013, r: -0.318). A statistically significant negative correlation was observed between the eosinophil-to-neutrophil ratio (ENR) and NIHSS score (p < 0.017, r: -0.305) as well as between ENR and symptom duration (p < 0.034, r: -0.271). Hemoglobin is a significant predictor of mortality in the logistic regression model (p < 0.05, CI: 0.253-0.942). For each one-unit increase in hemoglobin, the odds of mortality decrease by a factor of 0.488. Conclusion Certain blood cell types (neutrophils, eosinophils, and lymphocytes) play an active role in determining stroke prognosis. A detailed explanation of the role of leukocyte types lays the foundation for \"immunomodulation,\" which could be a promising novel treatment modality for future stroke patients.
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  • 文章类型: Journal Article
    嗜酸性粒细胞性胃炎和嗜酸性粒细胞性十二指肠炎(EoG/EoD)通常被误诊为功能性胃肠道(GI)疾病。因此,胃肠道症状为EoG/EoD的患者可能没有接受必要的诊断步骤.我们研究了胃肠病学家对慢性病患者的评估,无法解释,对非处方药无反应的中度至重度胃肠道症状。
    我们在办公室实践中对202名董事会认证的胃肠病学家进行了横断面在线调查,社区医院,或学术机构。受访者已经在积极的临床实践中接受了3-35年的住院医师培训,他们大部分时间都花在直接治疗病人上,管理≥1例肠易激综合征和/或功能性消化不良患者,每月进行≥1次内窥镜检查。分析反应以确定EoG/EoD诊断和管理的障碍。
    受访者平均每年管理1880名患者;最常见的诊断是功能性消化不良(36%)和胃食管反流病(19%)。接受上内窥镜检查的患者的平均比例为42%至84%。从>90%的可见内窥镜粘膜异常患者和42%-72%的正常粘膜患者收集活检。大约20%的受访者仅从胃肠道的每个部位收集了1-2次活检。只有30%的人经常要求病理学家计数嗜酸性粒细胞,近40%的EoG/EoD诊断没有组织学阈值。
    胃肠病学家对慢性病患者的评估各不相同,不明原因的中度至重度胃肠道症状。有限的胃和十二指肠活检,特别是来自正常的粘膜,未能要求组织嗜酸性粒细胞计数可能导致EoG/EoD的诊断不足。EoG/EoD诊断指南的可用性和认识应提高临床实践中的检测。
    UNASSIGNED: Eosinophilic gastritis and eosinophilic duodenitis (EoG/EoD) are often misdiagnosed as functional gastrointestinal (GI) disorders. Consequently, patients with GI symptoms of EoG/EoD may not undergo the necessary steps for diagnosis. We studied gastroenterologists\' evaluations of patients with chronic, unexplained, moderate-to-severe GI symptoms that were unresponsive to over-the-counter medications.
    UNASSIGNED: We performed a cross-sectional online survey of 202 board-certified gastroenterologists at office-based practices, community hospitals, or academic institutions. Respondents had been in active clinical practice for 3-35 years post-residency training, spent most of their time on direct patient care, managed ≥1 patient with irritable bowel syndrome and/or functional dyspepsia, and performed ≥1 endoscopy per month. Responses were analyzed to identify barriers to EoG/EoD diagnosis and management.
    UNASSIGNED: Respondents managed a mean of 1880 patients per year; the most common diagnoses were functional dyspepsia (36%) and gastroesophageal reflux disease (19%). Mean proportions of patients who underwent upper endoscopy ranged from 42% to 84%. Biopsies were collected from >90% of patients with visible endoscopic mucosal abnormalities vs 42%-72% of patients with normal-appearing mucosae. Approximately 20% of respondents collected only 1-2 biopsies from each site of the GI tract. Only 30% routinely requested pathologists to count eosinophils, and nearly 40% had no histologic threshold for EoG/EoD diagnosis.
    UNASSIGNED: Gastroenterologists vary in their evaluation of patients with chronic, unexplained moderate-to-severe GI symptoms. Limited gastric and duodenal biopsy collection, particularly from normal-appearing mucosae, and failure to request tissue eosinophil counts might contribute to underdiagnosis of EoG/EoD. Availability and awareness of EoG/EoD diagnostic guidelines should improve detection in clinical practice.
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  • 文章类型: Journal Article
    背景:哮喘是一种慢性炎症性疾病,其特征是急性哮喘发作(AAE)。除了慢性气道炎症,这对受影响的患者和他们的父母都有巨大的影响。这项研究的主要目的是探索可用的白细胞衍生的炎症标志物在诊断AAE和识别需要进入儿科重症监护病房(PICU)的严重恶化风险的儿童中的实用性。
    方法:本研究为回顾性队列研究。回顾了128名被诊断为哮喘恶化的儿童和131名2至12岁的稳定哮喘儿童的医疗记录。
    结果:共有259名参与者入组。AAE患儿的白细胞计数显着升高(WBC:10.0±4.2×103/μLvs.7.1±2.2×103/μL,p<0.001),绝对中性粒细胞计数(ANC:7398.5±4600细胞/μLvs.2634.8±1448个细胞/μL,p<0.001),和中性粒细胞与淋巴细胞的比率(NLR:7.0±6.8与0.9±0.7,p<0.001),但绝对淋巴细胞计数显着降低(ALC:1794.1±1536×103/μLvs.3552.9±1509×103/μL,p<0.001)。有趣的是,血液嗜酸性粒细胞计数显示出相反的趋势:与经历恶化的儿童相比,稳定的哮喘儿童的嗜酸性粒细胞明显更多(370.1±342.7细胞/mm3vs.0.9±1.9细胞/mm3,p<0.001)。确定了指示AAE的两个标准:NLR值大于1.2,具有良好的辨别能力(曲线下面积[AUC]0.90;95%置信区间[CI]0.85-0.94;灵敏度82.5%;特异性79.5%),ANC值超过3866,具有中等辨别能力(AUC0.86;95%CI0.81-0.91;敏感性75.0%;特异性82.3%)。此外,这些标记的比较分析(NLR,ANC,PLR,WBC,AEC,AAE患者和ALC)在需要PICU入院的患者和不需要PICU的患者之间没有显着差异。
    结论:这项研究贡献了两个主要发现。首先是NLR,ANC,WBC,与稳定哮喘患者相比,AAE患者的PLR明显更高。第二个是与AAE相比,哮喘稳定儿童的AEC和ALC水平更高。此外,这项研究表明,所研究的标记(NLR,ANC,PLR,WBC,AEC,和ALC)没有区分需要PICU入院的AAE患者和普通病房的患者,这表明需要替代预测因素。
    BACKGROUND: Asthma is a chronic inflammatory condition characterized by episodes of acute asthma exacerbations (AAEs), in addition to chronic airway inflammation, which has a huge impact on both the affected patients and their parents. The main objective of this study was to explore the utility of available white-blood-cell-derived inflammatory markers in diagnosing AAEs and identifying children at risk for severe exacerbations requiring admission to the pediatric intensive care unit (PICU).
    METHODS: This study was a retrospective cohort study. The medical records of 128 children diagnosed with asthma exacerbation and 131 children with stable asthma between the ages of 2 and 12 years were reviewed.
    RESULTS: A total of 259 participants were enrolled. Children with AAE demonstrated significantly higher white blood cell counts (WBC: 10.0 ± 4.2 × 103/μL vs. 7.1 ± 2.2 × 103/μL, p < 0.001), absolute neutrophil counts (ANC: 7398.5 ± 4600 cells/μL vs. 2634.8 ± 1448 cells/μL, p < 0.001), and neutrophil-to-lymphocyte ratios (NLR: 7.0 ± 6.8 vs. 0.9 ± 0.7, p < 0.001) but significantly lower absolute lymphocyte counts (ALC: 1794.1 ± 1536 × 103/μL vs. 3552.9 ± 1509 × 103/μL, p < 0.001). Interestingly, blood eosinophil count displayed an opposite trend: children with stable asthma had significantly more eosinophils compared to those experiencing an exacerbation (370.1 ± 342.7 cells/mm3 vs. 0.9 ± 1.9 cells/mm3, p < 0.001). Two criteria that are indicative of AAE were identified: NLR values greater than 1.2, with good discriminative ability (area under the curve [AUC] 0.90; 95% confidence interval [CI] 0.85-0.94; sensitivity 82.5%; specificity 79.5%), and ANC values exceeding 3866, with moderate discriminative ability (AUC 0.86; 95% CI 0.81-0.91; sensitivity 75.0%; specificity 82.3%). Moreover, a comparative analysis of these markers (NLR, ANC, PLR, WBC, AEC, and ALC) in patients with AAE did not demonstrate significant differences between those requiring PICU admission and those who did not require it.
    CONCLUSIONS: This study contributes two major findings. The first is that NLR, ANC, WBC, and PLR are significantly higher in AAE patients compared to those with stable asthma. The second is that children with stable asthma have higher AEC and ALC levels compared to those with AAE. Furthermore, this study has revealed that the studied markers (NLR, ANC, PLR, WBC, AEC, and ALC) did not differentiate between AAE patients requiring PICU admission and those managed in the general ward, suggesting a need for alternative predictive factors.
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  • 文章类型: Journal Article
    背景:嗜酸性粒细胞是通过IL5(美泊利单抗)和IL5受体(贝那利珠单抗)阻断抑制的严重哮喘的关键治疗靶点。IL5通路生物制剂对最近描述的稳态(hEO)和炎性(iEO)嗜酸性粒细胞亚群的影响是未知的。我们旨在确定美泊利单抗和贝那利珠单抗治疗对嗜酸性粒细胞亚群和表型的相对影响。并探讨嗜酸性粒细胞亚群与重症哮喘特征和治疗反应的临床关联。
    方法:我们进行了严重哮喘的横断面观察研究(嗜酸性粒细胞n=32,非嗜酸性粒细胞n=23,美泊利单抗治疗n=25),在两个时间点对30名嗜酸性粒细胞参与者进行纵向随访(4-24周,>24周)开始使用美泊利单抗(n=20)或贝那利珠单抗(n=10)后。通过表面CD62L蛋白的流式细胞术评估来测量血液hEO和iEO。
    结果:在横断面和纵向研究中,接受mepolizumab治疗的参与者中iEO比例均显着降低。Mepolizumab和benralizumab消耗iEO的程度相似,然而,在随访时,mepolizumab参与者中的hEO数量显著增加.较高的iEO比例与嗜酸性粒细胞哮喘但非嗜酸性粒细胞哮喘的较差哮喘控制相关。在美泊利单抗治疗的个体中,较高的残留iEO比例与较差的哮喘控制相关。在大约一半的接受mepolizumab治疗的参与者中观察到血液嗜酸性粒细胞活力降低。这与明显更好的哮喘控制和肺活量测定相关。
    结论:Mepolizumab可在重度哮喘中消耗iEO并降低循环嗜酸性粒细胞活力,但保留了循环hEO的残留群体。相反,贝那利珠单抗耗尽了iEO和hEO。较高的iEO丰度和嗜酸性粒细胞活力与美泊利单抗治疗后较差的临床结果相关。监测循环嗜酸性粒细胞表型和活力可能有助于预测重症哮喘的生物治疗反应。
    BACKGROUND: Eosinophils are key therapeutic targets in severe asthma that are suppressed by IL5 (mepolizumab) and IL5 receptor (benralizumab) blockade. The effect of IL5 pathway biologics on recently described homeostatic (hEOs) and inflammatory (iEOs) eosinophil subsets is unknown. We aimed to determine the relative impact of mepolizumab and benralizumab treatment on eosinophil subset and phenotype, and explore clinical associations of eosinophil subsets with severe asthma characteristics and treatment response.
    METHODS: We performed a cross-sectional observational study of severe asthma (eosinophilic n = 32, non-eosinophilic n = 23, mepolizumab-treated n = 25), with longitudinal follow-up of 30 eosinophilic participants at two timepoints (4-24 weeks, >24 weeks) post-commencement of mepolizumab (n = 20) or benralizumab (n = 10). Blood hEOs and iEOs were measured by flow cytometry assessment of surface CD62L protein.
    RESULTS: iEO proportion was significantly lower in mepolizumab-treated participants in both the cross-sectional and longitudinal study. Mepolizumab and benralizumab depleted iEOs to a similar extent, however a significantly greater number of hEOs remained in mepolizumab participants at follow-up. Greater iEO proportion correlated with poorer asthma control in eosinophilic but not non-eosinophilic asthma. Higher residual iEO proportion correlated with poorer asthma control in mepolizumab-treated individuals. Reduced blood eosinophil viability was observed in around half of mepolizumab-treated participants, which was associated with significantly better asthma control and spirometry.
    CONCLUSIONS: Mepolizumab depletes iEOs and reduces circulating eosinophil viability in severe asthma but preserves a residual population of circulatory hEOs. In contrast benralizumab depleted both iEOs and hEOs. Higher iEO abundance and eosinophil viability are associated with poorer clinical outcomes following mepolizumab-treatment. Monitoring circulating eosinophil phenotype and viability may be useful to predict biologic treatment response in severe asthma.
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  • 文章类型: Journal Article
    嗜酸性粒细胞胃肠道疾病研究人员联盟(CEGIR)和国际胃肠道嗜酸性粒细胞研究人员(TIGERS)在2024年美国过敏学会年会上组织了为期一天的研讨会,哮喘与免疫学。研讨会在基础和转化研究以及关于嗜酸性粒细胞性胃肠道疾病(EGID)的机制和管理的辩论方面取得了新发现。还介绍了最近的临床试验和共识指南的更新。在这里,我们总结了在研讨会上介绍的有关EGID的最新情况。
    The Consortium of Eosinophilic Gastrointestinal disease Researchers (CEGIR) and The International Gastrointestinal Eosinophil Researchers (TIGERS) organized a day-long symposium at the 2024 Annual Meeting of the American Academy of Allergy, Asthma & Immunology. The symposium featured new discoveries in basic and translational research and debates on the mechanisms and management of eosinophilic gastrointestinal diseases (EGIDs). Updates on recent clinical trials and consensus guidelines were also presented. Herein, we summarize the updates on EGIDs presented at the symposium.
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  • 文章类型: Journal Article
    特应性皮炎(AD)由于其病因知之甚少而提出了重大的治疗挑战。嗜酸性粒细胞增多,过敏性炎症的标志,与AD发病机制有关。产生白细胞介素-10(IL-10)的调节性B(Breg)细胞表现出有效的抗炎作用。然而,它们在控制AD相关嗜酸性粒细胞增多中的作用尚不清楚.探讨嗜酸性粒细胞对AD的影响,我们采用了IL-5Rα缺陷型(Il5ra-/-)小鼠,缺乏功能性嗜酸性粒细胞。在这些小鼠中诱导AD导致减轻的疾病症状,强调嗜酸性粒细胞在AD发展中的关键作用。此外,将纯化的Breg细胞过继转移到患有AD的小鼠中可显着减轻疾病的严重程度。机制研究表明,Breg细胞产生的IL-10直接抑制嗜酸性粒细胞活化和向皮肤的浸润。体外实验进一步证实Breg细胞以IL-10依赖性方式抑制嗜酸性粒细胞过氧化物酶分泌。我们的集体发现表明,来自Breg细胞的IL-10通过抑制嗜酸性粒细胞活化和组织浸润来减轻AD。本研究阐明了Breg细胞的一种新的调控机制,为未来Breg介导的AD治疗策略奠定基础。
    Atopic dermatitis (AD) presents significant therapeutic challenges due to its poorly understood etiology. Eosinophilia, a hallmark of allergic inflammation, is implicated in AD pathogenesis. Interleukin-10 (IL-10)-producing regulatory B (Breg) cells exhibit potent anti-inflammatory effects. However, their role in controlling AD-related eosinophilia is not well understood. To investigate the impact of eosinophils on AD, we employed IL-5Rα-deficient (Il5ra-/-) mice, which lack functional eosinophils. Induction of AD in these mice resulted in attenuated disease symptoms, underscoring the critical role of eosinophils in AD development. Additionally, the adoptive transfer of purified Breg cells into mice with AD significantly alleviated disease severity. Mechanistic studies revealed that IL-10 produced by Breg cells directly inhibits eosinophil activation and infiltration into the skin. In vitro experiments further confirmed that Breg cells inhibited eosinophil peroxidase secretion in an IL-10-dependent manner. Our collective findings demonstrate that IL-10 from Breg cells alleviates AD by suppressing eosinophil activation and tissue infiltration. This study elucidates a novel regulatory mechanism of Breg cells, providing a foundation for future Breg-mediated therapeutic strategies for AD.
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  • 文章类型: Journal Article
    细胞溶解性ETosis是一种不同于细胞凋亡和坏死的程序性细胞死亡,在先天免疫系统和疾病进展中起着重要作用。经由过程ETosis,细胞将它们的染色质与不同的抗菌蛋白释放到细胞外环境中,形成细胞外陷阱(ETs)。尽管已经报道了几种白细胞类型的ETosis,很少有研究比较ETosis和白细胞中ET的组成蛋白。这项研究的目的是更好地了解嗜酸性粒细胞ETosis(EETosis)与其他白细胞相比的特征。我们分离了人血嗜酸性粒细胞,中性粒细胞,嗜碱性粒细胞,单核细胞,和淋巴细胞,并用已知的ETosis诱导剂刺激它们,蛋白激酶C激活剂PMA,或者钙离子载体A23187.刺激180分钟后,两种刺激均以NADPH氧化酶依赖性方式诱导嗜酸性粒细胞死亡和ET释放。PMA还在中性粒细胞中诱导NADPH-氧化酶依赖性ETosis,而在嗜碱性粒细胞中很少或没有观察到显著的ETosis,单核细胞,或淋巴细胞在180分钟。基于质谱的嗜酸性粒细胞和嗜中性粒细胞衍生的ET的蛋白质组学分析鉴定出997和1415种蛋白质,分别。在测试的生理刺激中,固定化IgA和IgG诱导的脑电图。C-C基序趋化因子配体11(CCL11)和白细胞介素5(IL-5)是EETosis的弱诱导因子,但是共刺激显著诱导了快速的EETosis。在高血清或白蛋白条件下,与CCL11和IL-5的共刺激通过防止自发凋亡来矛盾地延长细胞存活。这项研究提供了对EETosis的深入表征,并强调了嗜酸性粒细胞存活和细胞死亡途径的精确调节。
    Cytolytic ETosis is a type of programmed cell death distinct from apoptosis and necrosis and plays a major role in the innate immune system and disease progression. Through the process of ETosis, cells release their chromatin with diverse antimicrobial proteins into the extracellular milieu, forming extracellular traps (ETs). Although ETosis has been reported in several leukocyte types, few studies have compared ETosis and the component proteins of ETs in leukocytes. The aim of this study was to better understand the characteristics of eosinophil ETosis (EETosis) compared with other leukocytes. We isolated human blood eosinophils, neutrophils, basophils, monocytes, and lymphocytes and stimulated them with known ETosis inducers, a protein kinase C activator PMA, or a calcium ionophore A23187. Both stimuli induced eosinophil cell death and ET release after 180 minutes of stimulation in a NADPH-oxidase-dependent manner. PMA also induced NADPH-oxidase-dependent ETosis in neutrophils, whereas little or no significant ETosis was observed in basophils, monocytes, or lymphocytes at 180 minutes. Mass spectrometry-based proteomic analysis of eosinophil- and neutrophil-derived ETs identified 997 and 1415 proteins, respectively. Among the physiological stimuli tested, immobilized IgA and IgG induced EETosis. C-C motif chemokine ligand 11 (CCL11) and interleukin 5 (IL-5) were weak inducers of EETosis, but co-stimulation significantly induced rapid EETosis. Under high serum or albumin conditions, co-stimulation with CCL11 and IL-5 paradoxically prolonged cell survival by preventing spontaneous apoptosis. This study provides an in-depth characterization of EETosis and highlights the precise regulation of eosinophil survival and cell death pathways.
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  • 文章类型: Journal Article
    嗜酸性粒细胞在气道炎症和哮喘发病机制中的作用已被确定。血液和痰中嗜酸性粒细胞计数升高与疾病严重程度和哮喘恶化风险增加相关。相反,也有初步证据表明气道中嗜酸性粒细胞的抗病毒特性。嗜酸性粒细胞的这些双重作用尤其相关,因为呼吸道病毒感染会导致哮喘恶化。针对与嗜酸性粒细胞相关病理有关的关键分子的生物疗法已在重度哮喘患者中获得批准,因此,临床中消耗嗜酸性粒细胞的作用引起了人们的极大兴趣.本文综述了嗜酸性粒细胞在哮喘和急性发作中的病理和抗病毒作用。我们还强调了使用生物疗法的哮喘急性发作的显着减少,即使在呼吸道病毒季节的高峰期。此外,我们讨论了这些发现与嗜酸性粒细胞在哮喘中呼吸道病毒感染的炎症和抗病毒反应中的作用有关的意义。
    The role of eosinophils in airway inflammation and asthma pathogenesis is well established, with raised eosinophil counts in blood and sputum associated with increased disease severity and risk of asthma exacerbation. Conversely, there is also preliminary evidence suggesting antiviral properties of eosinophils in the airways. These dual roles for eosinophils are particularly pertinent as respiratory virus infections contribute to asthma exacerbations. Biologic therapies targeting key molecules implicated in eosinophil-associated pathologies have been approved in patients with severe asthma and, therefore, the effects of depleting eosinophils in a clinical setting are of considerable interest. This review discusses the pathological and antiviral roles of eosinophils in asthma and exacerbations. We also highlight the significant reduction in asthma exacerbations seen with biologic therapies, even at the height of the respiratory virus season. Furthermore, we discuss the implications of these findings in relation to the role of eosinophils in inflammation and antiviral responses to respiratory virus infection in asthma.
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  • 文章类型: Journal Article
    背景:COPD加重是发病率和死亡率的主要原因。虽然吸入性皮质类固醇(ICS)具有长期治疗作用,它们在恶化中的功效,特别是作为全身性类固醇的辅助药物,尚不清楚。
    方法:在这项回顾性观察研究中,我们分析了2018年1月至2023年1月在以色列三级医疗中心接受COPD加重治疗的870名受试者的数据.我们调查了在标准全身性类固醇治疗中添加ICS对住院时间的影响,插管率,和30天死亡率,使用倾向得分匹配来解释混杂因素。
    结果:队列,匹配后,包括354名接受全身性类固醇和ICS治疗的受试者和121名单独接受全身性类固醇治疗的受试者。两组之间的所有特征相似。我们的分析显示30天死亡率没有差异(7.1%vs5.8%,P=0.63)或次要结果(插管,住院时间,和再入院率)。基于不同嗜酸性粒细胞水平的亚组分析没有改变这些发现。在一般队列的多变量分析中,嗜酸性粒细胞计数<150个细胞/μL(调整比值比0.45[95%CI0.21-0.87],P=.02)和高Charlson得分(调整后的赔率比1.19[95%CI1.02-1.37],P=.02)是30天死亡率的独立预测因子。
    结论:尽管已知ICS治疗慢性COPD的益处,我们没有发现ICS对加重期全身性类固醇的附加价值.这些结果强调了个体化治疗策略和进一步研究ICS在COPD加重中的作用的必要性。
    BACKGROUND: COPD exacerbations are a major cause of morbidity and mortality. Although inhaled corticosteroids (ICS) have a role as long-term treatment, their efficacy in exacerbations, particularly as an adjunct to systemic steroids, remains unclear.
    METHODS: In this retrospective observational study, we analyzed data from 870 subjects admitted with COPD exacerbations to a tertiary medical center in Israel from January 2018-January 2023. We investigated the impact of adding ICS to standard systemic steroid treatment on hospital length of stay, intubation rates, and 30-d mortality using propensity score matching to account for confounders.
    RESULTS: The cohort, after matching, included 354 subjects treated with systemic steroids and ICS and 121 treated with systemic steroids alone. All characteristics were similar between the groups. Our analysis showed no differences in 30-d mortality (7.1% vs 5.8%, P = .63) or secondary outcomes (intubation, hospital length of stay, and readmission rates) between the groups. Subgroup analyses based on different eosinophil levels did not alter these findings. In multivariate analysis among the general cohort, eosinophil count < 150 cells/μL (adjusted odds ratio 0.45 [95% CI 0.21-0.87], P = .02) and high Charlson score (adjusted odds ratio 1.19 [95% CI 1.02-1.37], P = .02) were independent predictors for 30-d mortality.
    CONCLUSIONS: Despite the known benefits of ICS in managing chronic COPD, we did not find an added value of ICS to systemic steroids in exacerbations. These results underscore the necessity for individualized treatment strategies and further research into the role of ICS in COPD exacerbations.
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