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High mobility group box protein 1 sensitizes mononuclear cells to further contact with lipopolysaccharide. 高迁移率基团盒蛋白 1 可使单核细胞进一步接触脂多糖。
IF 1.3 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-04-19 DOI: 10.5114/ceji.2024.138600
Jakub Piotrowski, Tomasz Jędrzejewski

Fever is an adaptive host-defense response to infection and nowadays is rightly considered to be an expression of a healthy body and a well-functioning immune system. The condition is that it must be tightly regulated. Therefore, in individual cases, fever may be detrimental and should be treated. Specific excessive febrile reaction to pathogens which occurs after aseptic injuries is one among such cases. We previously found that among necrotic products, high mobility group box protein 1 (HMGB1) released from the site of aseptic injury affects immune effectors (cells) to mediate higher fever in response to further contact with bacterial lipopolysaccharide (LPS). Here we observed that intraperitoneal (i.p.) pre-injection of recombinant HMGB1 (5 µg/rat i.p.) provoked an increase in plasma levels of prostaglandin E2 (PGE2) in rats and augmented release of interleukin (IL)-1β and IL-6 after LPS administration at a dose of 50 µg/kg i.p. compared to rats pre-injected with saline or heat-denatured HMGB1. Furthermore, peripheral blood mononuclear cells (PBMCs) isolated from rats injected with HMGB1 were more sensitized to produce enhanced levels of IL-1β and PGE2 when stimulated with LPS in vitro (1 µg/ml/106 cells for 4 h) compared to control animals injected with saline or heat-denatured HMGB1. We also noted a significant increase in activation of nuclear factor κB (NF-κB) in cells isolated from rats injected with HMGB1. Altogether, the obtained results suggest that HMGB1 participates in priming of immune cells to further contact with pathogens.

发烧是宿主对感染的一种适应性防御反应,如今被正确地认为是健康身体和免疫系统功能良好的表现。但条件是必须严格控制发烧。因此,在个别情况下,发热可能是有害的,应予以治疗。无菌性损伤后出现的对病原体的特异性过度发热反应就是其中之一。我们以前曾发现,在坏死产物中,无菌损伤部位释放的高迁移率基团盒蛋白 1(HMGB1)会影响免疫效应因子(细胞),从而在进一步接触细菌脂多糖(LPS)时引起发热。我们在此观察到,与预先注射生理盐水或热变性 HMGB1 的大鼠相比,腹腔内预先注射 50 µg/kg 剂量的重组 HMGB1(5 µg/只大鼠)会引起大鼠血浆中前列腺素 E2(PGE2)水平的升高,并在注射 LPS 后增加白细胞介素(IL)-1β 和 IL-6 的释放。此外,与注射生理盐水或热变性 HMGB1 的对照组动物相比,从注射 HMGB1 的大鼠体内分离出的外周血单核细胞(PBMCs)在体外受到 LPS 刺激(1 µg/ml/106 个细胞,持续 4 小时)时更容易产生更高水平的 IL-1β 和 PGE2。我们还注意到,从注射了 HMGB1 的大鼠体内分离出来的细胞中,核因子 κB(NF-κB)的活化程度明显增加。总之,研究结果表明,HMGB1 参与了免疫细胞与病原体的进一步接触。
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引用次数: 0
A case of trigeminal neuralgia that occurred after COVID-19 vaccination. 接种 COVID-19 疫苗后出现三叉神经痛的病例。
IF 1.5 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-08-26 DOI: 10.5114/ceji.2024.142414
Zeliha Ünlü, İlhan Celil Özbek
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引用次数: 0
Preventive effect of hyperforin on lipopolysaccharide-induced acute kidney injury and inflammation by repressing the NF-κB/miR-21 axis. 金丝桃素通过抑制NF-κB/miR-21轴对脂多糖诱发的急性肾损伤和炎症有预防作用
IF 1.5 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-06-17 DOI: 10.5114/ceji.2024.140636
Haozhe Fan, Xiao He, Hongjie Tong, Kun Chen

Introduction: Hyperforin (HYP) has been reported to alleviate the inflammatory response. The purpose of this study was to examine the pharmacological effects of HYP on lipopolysaccharide (LPS)-induced inflammation and acute kidney injury (AKI).

Material and methods: In vitro and in vivo septic models were created using LPS-stimulated mice podocytes and LPS-injected mice. HYP (20 mg/kg/day) or antagomiR-21 (20 nM/0.1 ml; twice/week) was administered to mitigate LPS-induced AKI and podocyte apoptosis.

Results: HYP demonstrated potential as an NF-κB inhibitor, leading to enhanced survival rates in septic mice. Moreover, HYP directly hindered LPS-induced podocyte apoptosis and AKI. The underlying mechanism involves the modulation of LPS-induced transactivation of miR-21 by NF-κB. It was observed that excessive activation of the NF-κB/miR-21 signaling axis contributed to LPS-induced podocyte apoptosis and AKI. Additionally, the absence of miR-21 expression resulted in decreased LPS-induced podocyte apoptosis and amelioration of LPS-induced renal tubular injury.

Conclusions: The renoprotective effects of HYP were observed in septic mice through the inhibition of NF-κB/p65-mediated transactivation of miR-21. These findings suggest that targeting the NF-κB-miR-21 axis could be a potential therapeutic strategy for HYP in the prevention of AKI.

简介据报道,高良姜素(HYP)可减轻炎症反应。本研究旨在探讨 HYP 对脂多糖(LPS)诱导的炎症和急性肾损伤(AKI)的药理作用:材料和方法:使用 LPS 刺激的小鼠荚膜细胞和注射 LPS 的小鼠建立体外和体内败血症模型。给小鼠注射 HYP(20 毫克/千克/天)或 antagomiR-21(20 毫微克/0.1 毫升;两次/周)以减轻 LPS 诱导的 AKI 和荚膜细胞凋亡:结果:HYP 显示出作为 NF-κB 抑制剂的潜力,从而提高了脓毒症小鼠的存活率。此外,HYP 还能直接抑制 LPS 诱导的荚膜细胞凋亡和 AKI。其基本机制涉及 NF-κB 对 LPS 诱导的 miR-21 转录激活的调节。研究观察到,NF-κB/miR-21 信号轴的过度激活导致了 LPS 诱导的荚膜细胞凋亡和 AKI。此外,缺失 miR-21 的表达可减少 LPS 诱导的荚膜细胞凋亡,并改善 LPS 诱导的肾小管损伤:结论:HYP通过抑制NF-κB/p65介导的miR-21转录,对脓毒症小鼠具有肾保护作用。这些研究结果表明,靶向 NF-κB-miR-21 轴可能是 HYP 预防 AKI 的一种潜在治疗策略。
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引用次数: 0
Reference values of lymphocyte subsets from healthy Polish adults. 健康波兰成年人淋巴细胞亚群的参考值。
IF 1.3 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-03-22 DOI: 10.5114/ceji.2024.136371
Aleksander Roszczyk, Michał Zych, Dariusz Sołdacki, Radoslaw Zagozdzon, Monika J Kniotek

The flow cytometry method could support physicians' decisions in the diagnosis and treatment monitoring of immunodeficient patients. Most clinical recommendations are focused on the search for alterations in T- and B-lymphocyte subsets, less commonly natural killer (NK) cells and granulocytes. While reference values for clinically meaningful lymphocyte subsets have been published ubiquitously among numerous countries, we have not found significant data for a population of adult Polish habitats; thus we determined reference values for T, B, and NK subsets according to sex and age. The female group showed a higher percentage of lymphocytes (CD45++), T helper lymphocytes with a higher absolute count, as well as CD4/CD8 ratio, marginal zone-like B cells, class-switched B cells, and CD21low B cells than the male group. The male group was found to have elevated percentages of naïve B lymphocytes, transitional B cells, and plasmablasts. A weak positive correlation with age was found among double positive T lymphocytes, natural killer T cells (NKT) lymphocytes, and CD21low B cells. A negative correlation with age for double negative T lymphocytes, marginal zone-like B cells, and plasmablasts was noted. The results indicated the importance of creating distinct reference ranges regarding sex and age concerning immunophenotype.

流式细胞仪方法可以帮助医生对免疫缺陷患者进行诊断和治疗监测。大多数临床建议都侧重于寻找 T 淋巴细胞和 B 淋巴细胞亚群的变化,自然杀伤(NK)细胞和粒细胞的变化则不太常见。虽然许多国家都公布了具有临床意义的淋巴细胞亚群的参考值,但我们还没有找到波兰成年居民的重要数据;因此,我们根据性别和年龄确定了 T、B 和 NK 亚群的参考值。与男性相比,女性组的淋巴细胞(CD45++)、T 辅助淋巴细胞(绝对计数较高)、CD4/CD8 比率、边缘区样 B 细胞、类调换 B 细胞和 CD21 低 B 细胞的百分比较高。男性组的幼稚 B 淋巴细胞、过渡性 B 细胞和浆细胞的百分比也较高。双阳性 T 淋巴细胞、自然杀伤 T 细胞(NKT)淋巴细胞和 CD21low B 细胞与年龄呈弱正相关。双阴性 T 淋巴细胞、边缘区样 B 细胞和浆细胞与年龄呈负相关。结果表明,就免疫表型而言,建立不同性别和年龄的参考范围非常重要。
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引用次数: 0
Transcriptome analysis of anaerobic glycolysis effects on Jurkat T cell proliferation. 无氧糖酵解对 Jurkat T 细胞增殖影响的转录组分析
IF 1.5 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-08-12 DOI: 10.5114/ceji.2024.142116
Ziyu Wang, Hongyang Wang, Qinghai Wang, Tao Huang, Chen Guo, Jianlei Ji, Meijie Su, Weijia Xu, Yanwei Cao, Zhen Dong

Introduction: To explore the effects of anaerobic glycolysis on Jurkat T cell proliferation and clarify the possible mechanism via transcriptomic analysis.

Material and methods: The monocarboxylate transporter 1 inhibitor AZD3965 was used to target and block the transmembrane transport of lactate, thereby inhibiting anaerobic glycolysis in Jurkat T cells. Then, genes with differential expression between treated and untreated cells were detected by transcriptomic analysis, and constructs were generated. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses as well as protein-protein interaction (PPI) network analysis were performed to explore the potential mechanism.

Results: Inhibition of anaerobic glycolysis reduced Jurkat T-cell proliferation. RNA sequencing identified 1723 transcripts that were differentially expressed, including 1460 upregulated genes and 263 downregulated genes. GO functional enrichment analysis showed that the differentially expressed genes were mainly involved in the biological processes of response to unfolded protein, response to topologically incorrect protein, and protein folding. KEGG pathway analysis of differentially expressed genes or hub genes from the PPI network analysis revealed enrichment in the estrogen signaling and PI3K-Akt pathways.

Conclusions: Anaerobic glycolysis contributes to the regulation of Jurkat T-cell proliferation. The underlying mechanism may involve the estrogen signaling pathway or PI3K-Akt signaling pathway as well as protein metabolism.

引言探讨无氧糖酵解对 Jurkat T 细胞增殖的影响,并通过转录组分析阐明其可能的机制:利用单羧酸盐转运体1抑制剂AZD3965靶向阻断乳酸的跨膜转运,从而抑制Jurkat T细胞的无氧糖酵解。然后,通过转录组分析检测处理过和未处理过的细胞中表达不同的基因,并生成构建体。为了探索潜在的机制,还进行了基因本体(GO)和京都基因组百科全书(KEGG)通路分析以及蛋白质相互作用(PPI)网络分析:结果:抑制无氧糖酵解可减少Jurkat T细胞的增殖。RNA测序发现了1723个差异表达的转录本,包括1460个上调基因和263个下调基因。GO功能富集分析表明,差异表达的基因主要涉及对未折叠蛋白的反应、对拓扑结构不正确蛋白的反应和蛋白质折叠等生物学过程。对差异表达基因或PPI网络分析中的枢纽基因进行的KEGG通路分析显示,雌激素信号通路和PI3K-Akt通路中的差异表达基因较多:结论:无氧糖酵解有助于调节Jurkat T细胞的增殖。结论:无氧糖酵解有助于调节 Jurkat T 细胞的增殖,其潜在机制可能涉及雌激素信号通路或 PI3K-Akt 信号通路以及蛋白质代谢。
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引用次数: 0
The challenge of diagnosing and classifying eosinophilia and eosinophil disorders: A review. 嗜酸性粒细胞增多症和嗜酸性粒细胞失调症的诊断和分类难题:综述。
IF 1.3 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-04-19 DOI: 10.5114/ceji.2024.136512
Agnieszka Szymczyk, Jakub Jaworski, Monika Podhorecka

Eosinophilia is a feature of multiple conditions, both hematologic and non-hematologic, and may be associated with organ damage. The pathogenesis of eosinophilia can follow two distinct pathways. Primary eosinophilia is caused by a cell-intrinsic mechanism originating from clonal expansion of eosinophils through acquisition of a somatic mutation, such as FIP1L1-PDGFRA. In recent years, great progress has been made in the field of pathogenesis and molecularly targeted therapy of neoplastic eosinophilia. The diagnostic procedure should include, among other things, morphologic analysis of blood and bone marrow samples, cytogenetics and fluorescence in situ-hybridization tests to detect evidence of an acute or chronic myeloid or lymphoid disorder. Secondary eosinophilia follows a cell-extrinsic mechanism as a response to exogenous cytokines. In most clinical cases, peripheral blood eosinophilia is reactive and typically associated with non-hematological disorders such as infections, allergic conditions, connective tissue disorders, vasculitis, malignancy, or endocrinopathies. Nonetheless, the cause of most cases of hypereosinophilic syndrome remains unknown. In this article, we present a short review focused on differential diagnosis of eosinophilia and eosinophilic disorders. The diagnosis of eosinophilia is a challenge for physicians; thus this review may be useful in clinical practice.

嗜酸性粒细胞增多是血液病和非血液病等多种疾病的特征之一,可能与器官损伤有关。嗜酸性粒细胞增多症的发病机制有两种不同的途径。原发性嗜酸性粒细胞增多症是由细胞内在机制引起的,源于嗜酸性粒细胞通过获得体细胞突变(如 FIP1L1-PDGFRA)而导致的克隆性扩增。近年来,在肿瘤性嗜酸性粒细胞增多症的发病机制和分子靶向治疗领域取得了重大进展。诊断程序应包括血液和骨髓样本的形态学分析、细胞遗传学和荧光原位杂交试验等,以检测急性或慢性髓系或淋巴系统疾病的证据。继发性嗜酸性粒细胞增多是对外源性细胞因子的反应,是一种细胞外在机制。在大多数临床病例中,外周血嗜酸性粒细胞增多是反应性的,通常与非血液病有关,如感染、过敏性疾病、结缔组织病、血管炎、恶性肿瘤或内分泌病。然而,大多数嗜酸性粒细胞过多综合征病例的病因仍然不明。本文将对嗜酸性粒细胞增多症和嗜酸性粒细胞疾病的鉴别诊断进行简要综述。对医生来说,嗜酸性粒细胞增多症的诊断是一项挑战;因此,这篇综述可能对临床实践有所帮助。
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引用次数: 0
An updated review of immunotherapy in esophageal cancer: PD-L1 footprint. 食管癌免疫疗法最新综述:PD-L1足迹
IF 1.3 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-05-09 DOI: 10.5114/ceji.2024.139269
Juan Yao, Xiaoyan Tan, Yanping Sha, Yurao Chen, Ronghuai Chen, Dongping Shi

Esophageal cancer is considered one of the most significant challenges to public health worldwide. While various therapeutic options exist for esophageal cancer, including chemotherapy, radiotherapy, and surgery, several adverse effects of these medications have been reported. Therefore, a new generation of therapeutic lines should be applied to minimize complications. In this regard, immunotherapy is a novel approach that aims to kill tumor cells directly by targeting them. Specifically, monoclonal antibodies can target specific markers of esophageal cancer tumor cells, keeping other normal cells safe. Multiple monoclonal antibodies optimized for esophageal cancer, such as pembrolizumab, ramucirumab, trastuzumab, nivolumab, and ipilimumab, are available. On the other hand, esophageal cancer tumor cells express a specific inhibitory ligand and its receptor called programmed cell death, which can suppress T cell immune responses. This receptor provides an inhibitory signal, causing the highest expression of the PD-L1 ligand on tumor cells. The outcomes of this interaction lead to the suppression of the activation and function of T lymphocytes. Therefore, immunotherapy for esophageal cancer targeting the PD-1/PD-L1 pathway has shown a remarkable correlation with cancer care. This study presents a comprehensive review of the latest findings related to immunotherapy in esophageal cancer.

食道癌被认为是全球公共卫生面临的最重大挑战之一。虽然食管癌的治疗方法多种多样,包括化疗、放疗和手术,但有报道称这些药物会产生一些不良反应。因此,应采用新一代的治疗方法来减少并发症。在这方面,免疫疗法是一种新方法,旨在通过靶向肿瘤细胞直接杀死肿瘤细胞。具体来说,单克隆抗体可以靶向食管癌肿瘤细胞的特定标记物,同时保证其他正常细胞的安全。目前已有多种针对食管癌的单克隆抗体,如pembrolizumab、ramucirumab、曲妥珠单抗、nivolumab和ipilimumab。另一方面,食管癌肿瘤细胞表达一种特异性抑制配体及其受体,称为程序性细胞死亡,可抑制 T 细胞免疫反应。这种受体提供抑制信号,导致肿瘤细胞上的 PD-L1 配体表达量最高。这种相互作用的结果导致 T 淋巴细胞的活化和功能受到抑制。因此,针对 PD-1/PD-L1 通路的食管癌免疫疗法与癌症治疗有着显著的相关性。本研究全面综述了与食管癌免疫疗法相关的最新研究成果。
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引用次数: 0
Comparison of cytotoxicity methods for studying Vipera ammodytes venom and the anticytotoxic potency of antivenom. 比较研究蝰蛇毒液的细胞毒性方法和抗蛇毒血清的抗毒性效力。
IF 1.5 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-08-26 DOI: 10.5114/ceji.2024.142417
Ivana Lukic, Veljko Blagojevic, Rajna Minic, Sasa Ivanovic, Suncica Borozan, Vitomir Cupic, Irena Zivkovic

Introduction: Alternative in vitro tests that can be used instead of animal experiments are those that can most closely evaluate the biological activity of the drug of interest. For testing the potency of antivenom, these are the methods used to assess cytotoxicity. The aim of this study was to evaluate the most commonly used cytotoxicity methods for determining the protective potency of the antivenom Viekvin, which neutralizes Vipera ammodytes venom.

Material and methods: The selected methods are based on different biological mechanisms: MTT assay, based on the activity of cell oxidoreductase enzymes; crystal violet staining, based on the degree of cell adhesion; trypan blue staining, based on cell membrane permeability, and propidium iodide staining, based on measurement of nucleic acids of dead cells. The pro-apoptotic effect of the venom was also determined with annexin V staining.

Results: The IC50 value of V. ammodytes venom obtained by these methods was very similar, while the EC50 values differed significantly.

Conclusions: We concluded that the choice of the method used to measure the anticytotoxic anti-venom potency depends on the immunogenicity of the venom components that cause cell death; for each venom/antivenom pair, it is necessary to select the appropriate assay separately, and at present, none of the standard cytotoxic methods can be universally applied to determine antivenom potency.

导言:可替代动物实验的体外试验是那些能最接近地评估相关药物生物活性的试验。在测试抗蛇毒血清的效力时,这些方法可用于评估细胞毒性。本研究的目的是评估最常用的细胞毒性方法,以确定中和蝰蛇毒液的抗蛇毒血清 Viekvin 的保护效力:所选方法基于不同的生物机制:MTT 试验基于细胞氧化还原酶的活性;水晶紫染色基于细胞粘附的程度;胰蓝染色基于细胞膜的通透性;碘化丙啶染色基于死亡细胞核酸的测量。此外,还利用附件素 V 染色法测定了毒液的促凋亡作用:结果:通过这些方法获得的蝰蛇毒液的 IC50 值非常相似,而 EC50 值则有很大差异:我们得出结论:选择哪种方法来测定抗毒血清的抗毒效力取决于导致细胞死亡的毒液成分的免疫原性;对于每种毒液/抗毒血清配对,有必要分别选择适当的测定方法,目前,没有一种标准的细胞毒性方法可以普遍用于测定抗毒血清的效力。
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引用次数: 0
Influence of dietary and lifestyle factors on levels of inflammatory markers (IL-6, IFN-γ and TNF-α) in obese subjects. 饮食和生活方式因素对肥胖者炎症指标(IL-6、IFN-γ 和 TNF-α)水平的影响。
IF 1.3 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-04-15 DOI: 10.5114/ceji.2024.138748
Ewelina Polak-Szczybyło, Jacek Tabarkiewicz

Introduction: The low-grade inflammation occurring in obese individuals leads to many diseases, including cardiovascular disease (CVD). Dietary patterns, food groups or nutrients in a well-balanced diet may reduce the level of pro-inflammatory markers and the risk of obesity-related morbidities. Our study aims to describe three cytokines in obese patients in relation to dietary habits, lifestyle and body composition.

Material and methods: Serum samples were collected from 84 obese adult volunteer subjects [body mass index (BMI) ≥ 30 kg/m2] to analyze the concentrations of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and interferon γ (IFN-γ). The subjects were tested by bioelectrical impedance analysis (BIA) and completed a three-day food diary and original questionnaire with the FFQ-6 food consumption frequency questionnaire.

Results and conclusions: Higher serum levels of IL-6 and IFN-γ were found in patients with atherosclerosis, but the group was too small for a reliable correlation. Subcutaneous but not visceral adipose tissue correlated positively with IL-6 levels. Dietary factors such as amount of sugars, including galactose and sucrose, in the diet and the frequency of consumption of sweet flavored dairy products correlated positively with the levels of IL-6 and TNF-α, while the frequency of alcohol consumption negatively correlated with the level of IL-6. The greater the frequency of sports, the higher was the level of IL-6. In obese individuals, the level of pro-inflammatory cytokines could predispose to atherosclerosis and is associated with dietary factors and lifestyle.

引言肥胖者体内的低度炎症会导致多种疾病,包括心血管疾病(CVD)。均衡饮食中的膳食模式、食物种类或营养成分可降低促炎症标志物的水平,减少与肥胖相关的发病风险。我们的研究旨在描述肥胖患者体内的三种细胞因子与饮食习惯、生活方式和身体成分的关系:收集了 84 名肥胖成年志愿者[体重指数(BMI)≥ 30 kg/m2]的血清样本,以分析白细胞介素 6(IL-6)、肿瘤坏死因子α(TNF-α)和干扰素γ(IFN-γ)的浓度。受试者接受了生物电阻抗分析(BIA)测试,并完成了为期三天的食物日记和原始问卷与 FFQ-6 食物消费频率问卷:结果和结论:发现动脉粥样硬化患者血清中的 IL-6 和 IFN-γ 水平较高,但由于群体太小,无法得出可靠的相关性。皮下脂肪组织而非内脏脂肪组织与 IL-6 水平呈正相关。饮食因素,如饮食中糖(包括半乳糖和蔗糖)的含量以及食用甜味乳制品的频率与 IL-6 和 TNF-α 的水平呈正相关,而饮酒频率与 IL-6 的水平呈负相关。运动频率越高,IL-6 水平越高。在肥胖者中,促炎细胞因子的水平可能导致动脉粥样硬化,并与饮食因素和生活方式有关。
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引用次数: 0
Biomarkers of type 2 and non-type 2 inflammation in asthma exacerbations. 哮喘恶化中的 2 型和非 2 型炎症生物标志物。
IF 1.5 4区 医学 Q4 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-07-12 DOI: 10.5114/ceji.2024.141345
Kosar M Ali, Nsar Jamal, Shukur Wasman Smail, Martin Lauran, Jonas Bystrom, Christer Janson, Kawa Amin

Introduction: In adult-onset asthma, two major endotypes have been proposed: T2 with eosinophilia and non-T2 characterised by neutrophils and interleukin (IL)-17. The objective of the study was to examine the endotype marker profile in patients with severe asthma who were hospitalized for exacerbations, with a focus on differentiating between viral and non-viral triggers.

Material and methods: Forty-nine patients with asthma, admitted for exacerbations, and 51 healthy controls (HCs) were recruited. We further categorized the exacerbated asthma patients into two groups: non-viral infected (n = 38) and viral infected (n = 11) groups. Blood was drawn and a nasopharyngeal swab taken at the time of admission and eosinophil numbers, eosinophil cationic protein (ECP), immuno- globulin E (IgE), tryptase and viral infection were determined. Additionally, levels of IL-17, IL-33 and IL-31 were assessed.

Results: The majority of patients had adult onset asthma (age of diagnosis, 42.8 ±16.1) with a duration of 7.7 ±10.8 years, 24.5% being atopic. Patients had higher levels of eosinophils, ECP and IgE than healthy controls (eosinophils, p = 0.003; ECP and IgE, p = 0.0001). Immunohistochemistry confirmed eosinophils as a source of ECP. Tryptase (p = 0.0001), IL-17 (p = 0.0005), IL-31 (p = 0.0001) and IL-33 (p = 0.0002) were also higher in patients than controls. ECP correlated with tryptase (r = 0.08, p = 0.62). IL-17 showed the best correlation with other mediators, including ECP (r = 0.35, p = 0.24), tryptase (r = 0.69, p = 0.0001), IgE (r = 0.50, p = 0.0001), IL-33 (r = 0.95, p = 0.0001) and IL-31 (r = 0.89, p = 0.0001). IgE, IL-17, and IL-31 had a high AUC when differentiating those with severe and non-severe asthma. The group with exacerbated viral infection showed elevated levels of serum IL-17 and IL-31 compared to the non-infected group.

Conclusions: Patients with asthmatic exacerbations were found to have higher levels of both T2 and non-T2 inflammatory markers than healthy controls. In the study, levels of IgE, IL-17, and IL-31 differentiated between patients with severe and non-severe asthma. The last two cytokines were also able to distinguish between exacerbated asthma caused by viral infection and exacerbated asthma caused by non-viral infection.

介绍:成人哮喘有两种主要内型:嗜酸性粒细胞增多的 T2 型和以中性粒细胞和白细胞介素 (IL)-17 为特征的非 T2 型。本研究的目的是检查因病情加重而住院的重症哮喘患者的内型标志物概况,重点是区分病毒和非病毒诱因:我们招募了 49 名因病情加重而住院的哮喘患者和 51 名健康对照者(HCs)。我们进一步将哮喘加重患者分为两组:非病毒感染组(38 人)和病毒感染组(11 人)。入院时抽血并采集鼻咽拭子,测定嗜酸性粒细胞数量、嗜酸性粒细胞阳离子蛋白(ECP)、免疫球蛋白 E(IgE)、胰蛋白酶和病毒感染情况。此外,还评估了 IL-17、IL-33 和 IL-31 的水平:大多数患者为成人哮喘(诊断年龄为 42.8 ± 16.1),病程为 7.7 ± 10.8 年,其中 24.5% 为特应性哮喘。与健康对照组相比,患者的嗜酸性粒细胞、ECP和IgE水平更高(嗜酸性粒细胞,p = 0.003;ECP和IgE,p = 0.0001)。免疫组化证实嗜酸性粒细胞是 ECP 的来源。患者体内的胰蛋白酶(p = 0.0001)、IL-17(p = 0.0005)、IL-31(p = 0.0001)和 IL-33(p = 0.0002)也高于对照组。ECP 与胰蛋白酶相关(r = 0.08,p = 0.62)。IL-17与其他介质的相关性最好,包括ECP(r = 0.35,p = 0.24)、胰蛋白酶(r = 0.69,p = 0.0001)、IgE(r = 0.50,p = 0.0001)、IL-33(r = 0.95,p = 0.0001)和IL-31(r = 0.89,p = 0.0001)。在区分重度和非重度哮喘患者时,IgE、IL-17 和 IL-31 的 AUC 较高。与未感染组相比,病毒感染加重组的血清IL-17和IL-31水平升高:结论:与健康对照组相比,哮喘加重患者的 T2 和非 T2 炎症标志物水平均较高。在这项研究中,IgE、IL-17 和 IL-31 的水平可区分严重哮喘和非严重哮喘患者。后两种细胞因子还能区分病毒感染引起的哮喘加重和非病毒感染引起的哮喘加重。
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Central European Journal of Immunology
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