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Amygdalin Improves Allergic Asthma via the Thymic Stromal Lymphopoietin–dendritic Cell–OX40 Ligand Axis in a Mouse Model 小鼠模型中苦杏仁苷通过胸腺基质淋巴生成素-树突状细胞ox40配体轴改善过敏性哮喘
4区 医学 Q4 ALLERGY Pub Date : 2023-11-07 DOI: 10.18502/ijaai.v22i5.13993
Wen Cui, Huan Zhou, Ya-zun Liu, Yan Yang, Yi-zhong Hu, Zhao-peng Han, Jian-er Yu, Zheng Xue
Asthma, characterized by persistent inflammation and increased sensitivity of the airway, is the most common chronic condition among children. Novel, safe, and reliable treatment strategies are the focus of current research on pediatric asthma. Amygdalin, mainly present in bitter almonds, has anti-inflammatory and immunoregulatory potential, but its effect on asthma remains uninvestigated. Here, the impact of amygdalin on the thymic stromal lymphopoietin (TSLP)–dendritic cell (DC)–OX40L axis was investigated. A BALB/c mouse model for allergic asthma was established using the ovalbumin-sensitization method. Amygdalin treatment was administered between days 21 and 27 of the protocol. Cell numbers and hematoxylin and eosin (H&E) staining in bronchoalveolar lavage fluid (BALF) were used to observe the impact of amygdalin on airway inflammation. TSLP, IL-4, IL-5, IL-13, and IFN-γ concentrations were determined via Enzyme-linked immunosorbent assay (ELISA). TSLP, GATA-3, and T-bet proteins were measured using western blotting. Cell-surface receptor expression on DCs (MHC II, CD80, and CD86) was assessed via flow cytometry. OX40L mRNA and protein levels were detected using western blotting and qRT-PCR, respectively. Amygdalin treatment attenuated airway inflammation decreased BALF TSLP levels, inhibited DC maturation, restrained TSLP-induced DC surface marker expression (MHCII, CD80, and CD86), and further decreased OX40L levels in activated DCs. This occurred together with decreased Th2 cytokine levels (IL-4, IL-5, and IL-13) and GATA3 expression, whereas Th1 cytokine (IFN-γ) levels and T-bet expression increased. Amygdalin thus regulates the Th1/Th2 balance through the TSLP–DC–OX40L axis to participate in inflammation development in the airways, providing a basis for potential allergic asthma treatments.
哮喘是儿童中最常见的慢性疾病,其特征是持续的炎症和气道敏感性增加。新颖、安全、可靠的治疗策略是当前儿童哮喘研究的重点。苦杏仁苷主要存在于苦杏仁中,具有抗炎和免疫调节潜能,但其对哮喘的作用尚未研究。本实验研究了苦杏仁苷对胸腺基质淋巴生成素(TSLP) -树突状细胞(DC) -OX40L轴的影响。 采用卵清蛋白致敏法建立BALB/c小鼠变应性哮喘模型。在方案的第21天至第27天之间给予苦杏仁苷治疗。采用支气管肺泡灌洗液(BALF)细胞计数及苏木精和伊红(H&E)染色观察苦杏仁苷对气道炎症的影响。采用酶联免疫吸附法(ELISA)测定TSLP、IL-4、IL-5、IL-13和IFN-γ浓度。western blotting检测TSLP、GATA-3和T-bet蛋白。流式细胞术检测dc细胞表面受体(MHC II、CD80和CD86)的表达。western blotting和qRT-PCR分别检测OX40L mRNA和蛋白水平。 苦杏仁苷治疗可减轻气道炎症,降低BALF TSLP水平,抑制DC成熟,抑制TSLP诱导的DC表面标志物(MHCII, CD80和CD86)表达,并进一步降低活化DC中的OX40L水平。与此同时,Th2细胞因子(IL-4、IL-5和IL-13)水平和GATA3表达降低,而Th1细胞因子(IFN-γ)水平和T-bet表达升高。 因此,苦杏仁苷通过TSLP-DC-OX40L轴调控Th1/Th2平衡,参与气道炎症的发展,为潜在的过敏性哮喘治疗提供基础。
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 A BALB/c mouse model for allergic asthma was established using the ovalbumin-sensitization method. Amygdalin treatment was administered between days 21 and 27 of the protocol. Cell numbers and hematoxylin and eosin (H&E) staining in bronchoalveolar lavage fluid (BALF) were used to observe the impact of amygdalin on airway inflammation. TSLP, IL-4, IL-5, IL-13, and IFN-γ concentrations were determined via Enzyme-linked immunosorbent assay (ELISA). TSLP, GATA-3, and T-bet proteins were measured using western blotting. Cell-surface receptor expression on DCs (MHC II, CD80, and CD86) was assessed via flow cytometry. OX40L mRNA and protein levels were detected using western blotting and qRT-PCR, respectively.
 Amygdalin treatment attenuated airway inflammation decreased BALF TSLP levels, inhibited DC maturation, restrained TSLP-induced DC surface marker expression (MHCII, CD80, and CD86), and further decreased OX40L levels in activated DCs. This occurred together with decreased Th2 cytokine levels (IL-4, IL-5, and IL-13) and GATA3 expression, whereas Th1 cytokine (IFN-γ) levels and T-bet expression increased.
 Amygdalin thus regulates the Th1/Th2 balance through the TSLP–DC–OX40L axis to participate in inflammation development in the airways, providing a basis for potential allergic asthma treatments.","PeriodicalId":14560,"journal":{"name":"Iranian journal of allergy, asthma, and immunology","volume":"72 5","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135475685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Combined Treatment of Progressive Encephalitis in an X-linked Agammaglobulinemia Patient x连锁无球蛋白血症患者进行性脑炎的综合治疗
4区 医学 Q4 ALLERGY Pub Date : 2023-11-07 DOI: 10.18502/ijaai.v22i5.13999
Marco Antonio Yamazaki-Nakashimada, Patricia Herrera-Mora, Alfonso Mahrx-Bracho, Gabriela López-Herrera, Juan Carlos Bustamante-Ogando, Selma Cecilia Scheffler-Mendoza
Most patients with X-linked agammaglobulinemia are susceptible to infections, while some cases also suffer from inflammatory or autoimmune complications. We describe a patient with progressive encephalitis who improved after the use of immunomodulatory treatment with corticosteroids, fluoxetine, and nitazoxanide. In most of the cases the evolution of the progressive encephalitis is complicated and catastrophic. Based on our experience and the review of the literature, we propose the use of this combined treatment to control this devastating complication.
大多数x连锁无球蛋白血症患者易受感染,而一些病例还患有炎症或自身免疫性并发症。我们描述了一位进行性脑炎患者,在使用皮质类固醇、氟西汀和硝唑尼特进行免疫调节治疗后病情有所改善。在大多数情况下,进行性脑炎的演变是复杂的和灾难性的。根据我们的经验和文献回顾,我们建议使用这种联合治疗来控制这种毁灭性的并发症。
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引用次数: 0
MicroRNA-29a-3p Accelerates Inflammatory Damage in Neonatal Pneumonia Via Targeting Krüppel-like Factor 4 MicroRNA-29a-3p通过靶向kr<s:1> ppel样因子4加速新生儿肺炎的炎症损伤
4区 医学 Q4 ALLERGY Pub Date : 2023-11-07 DOI: 10.18502/ijaai.v22i5.13994
Xiao Juan Xu, Wei Liu, ShiNa Liland
Neonatal pneumonia (NP) is a frequently occurring illness during the neonatal phase. The study investigated the molecular process and the role of microRNA (miR)-29a-3p in NP. Peripheral blood was collected from NP patients and healthy newborns. Human lung fibroblasts cell line (WI-38) were treated with lipopolysaccharide (LPS)) to establish a cellular model for NP. Then, miR-29a-3p and Krüppel-like Factor 4 (KLF4) levels were detected by RT-qPCR or Western blot. The relationship between miR-29a-3p and KLF4 was confirmed by dual luciferase reporter gene assay. Cell survival was assessed using the CCK-8 assay, whereas the levels of interleukin-6, tumor necrosis factor-α, and IL-1β were quantified using ELISA. Additionally, apoptosis was evaluated through flow cytometry. Meanwhile, Bax and Bcl-2 were detected by RT-qPCR. Neonatal rats were administered LPS intraperitoneally (3 mg/kg) to induce NP, and pathological injury and inflammatory reaction were analyzed. MiR-29a-3p was elevated but KLF4 was silenced in NP patient’s serum, LPS-treated WI-38 cell line, and LPS-treated newborn rats. Silence of miR-29a-3p or elevation of KLF4 constrained cell proliferation with inflammation of LPS-treated WI-38 cell line. MiR-29a-3p immediately targeted KLF4. Additionally, silence of miR-29a-3p alleviated LPS-stimulated lung injury and inflammation in neonatal rats. The protective action of silenced miR-29a-3p in LPS-treated WI-38 cell line and newborn rats was turned around by silencing KLF4. This study demonstrates originally that miR-29a-3p boosts inflammatory damage in NP via targeting KLF4, offering a basis for clinically diagnosing and treating NP.
新生儿肺炎(NP)是一种常见于新生儿期的疾病。本研究探讨了microRNA (miR)-29a-3p在NP中的分子过程和作用。采集NP患者和健康新生儿外周血。用脂多糖(LPS)处理人肺成纤维细胞(WI-38),建立NP细胞模型。然后采用RT-qPCR或Western blot检测miR-29a-3p和kr ppel样因子4 (KLF4)水平。双荧光素酶报告基因检测证实miR-29a-3p与KLF4的关系。使用CCK-8法评估细胞存活,而使用ELISA法定量白细胞介素-6、肿瘤坏死因子-α和IL-1β的水平。此外,流式细胞术检测细胞凋亡。同时RT-qPCR检测Bax和Bcl-2。采用LPS (3 mg/kg)腹腔诱导新生大鼠NP,观察病理损伤及炎症反应。 NP患者血清、lps处理的WI-38细胞系和lps处理的新生大鼠中MiR-29a-3p升高,KLF4沉默。miR-29a-3p的沉默或KLF4的升高抑制了lps处理的WI-38细胞系的细胞增殖和炎症。MiR-29a-3p立即靶向KLF4。此外,miR-29a-3p的沉默减轻了lps刺激的新生大鼠肺损伤和炎症。沉默miR-29a-3p对lps处理的WI-38细胞系和新生大鼠的保护作用通过沉默KLF4而逆转。 本研究初步证实miR-29a-3p通过靶向KLF4促进NP的炎症损伤,为NP的临床诊断和治疗提供依据。
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引用次数: 0
Cycle Threshold Values Predict COVID-19 Severity and Mortality but are not Correlated with Laboratory Markers 周期阈值预测COVID-19严重程度和死亡率,但与实验室标志物无关
4区 医学 Q4 ALLERGY Pub Date : 2023-11-07 DOI: 10.18502/ijaai.v22i5.13996
Behnaz Esmaeili, Hoda Khoshnevis, Atefe Alirezaee, Abbas Shakoori, Zahra Pourpak, Hamid Chegini, Zahra Ahmadinejad
Many studies have evaluated the possible utility of cycle threshold (Ct) values as a predictor of Coronavirus disease 2019 (COVID-19) severity and patient outcome. Given the inconsistent results, we aimed to evaluate the association between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Ct values and disease severity, inflammatory markers, and outcomes in Iranian patients with COVID-19. A retrospective study of 528 patients with COVID-19 hospitalized from September 2020 to October 2021 was conducted. Demographic, clinical, and laboratory data of patients were retrieved from electronic medical records. Ct values were analyzed as a continuous variable after subcategorizing into 3 groups: low (Ct values<20), medium (Ct values 20 to 30), and high (Ct values>30). Of the 528 patients (45.1% female) aged 13 to 97 years, 109 patients had low Ct values, 312 patients had medium, and 107 patients had high Ct values. Patients with low Ct values were more likely to present with critical COVID-19, require invasive mechanical ventilation and develop complications such as acute respiratory distress syndrome and pneumonia. Furthermore, patients with low or medium Ct values were more likely to die compared to patients with high Ct values.Multivariate analysis showed that patients with low or medium Ct values were more likely to have severe COVID-19 compared with patients with high Ct values. The multivariate analysis also showed a higher risk of mortality in patients with low Ct values compared to patients with high Ct values, although this was not statistically significant. Our findings revealed that Ct values were an independent predictor of COVID-19 severity. The risk of mortality was higher in patients with low Ct values. However, further investigation is needed to address the correlation between Ct values and inflammatory factors.
许多研究已经评估了周期阈值(Ct)作为2019冠状病毒病(COVID-19)严重程度和患者预后预测因子的可能效用。鉴于结果不一致,我们旨在评估伊朗COVID-19患者的严重急性呼吸综合征冠状病毒2 (SARS-CoV-2) Ct值与疾病严重程度、炎症标志物和结局之间的关系。 对2020年9月至2021年10月住院的528例新冠肺炎患者进行回顾性研究。从电子病历中检索患者的人口统计、临床和实验室数据。Ct值作为一个连续变量进行分析,将其细分为3组:低(Ct值<20)、中(Ct值20 ~ 30)、高(Ct值>30)。 528例患者(女性45.1%),年龄13 ~ 97岁,Ct值低109例,中312例,高107例。Ct值低的患者更容易出现重症COVID-19,需要有创机械通气,并发生急性呼吸窘迫综合征和肺炎等并发症。此外,与高Ct值的患者相比,低或中等Ct值的患者更容易死亡。多因素分析显示,与高Ct值的患者相比,低Ct值或中Ct值的患者更容易发生重症COVID-19。多变量分析还显示,与高Ct值的患者相比,低Ct值的患者死亡风险更高,尽管这没有统计学意义。 我们的研究结果显示,Ct值是COVID-19严重程度的独立预测因子。Ct值低的患者死亡风险较高。但Ct值与炎症因子的相关性有待进一步研究。
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引用次数: 0
Expression Analysis of Long Noncoding RNA-MALAT1 and Interleukin-6 in Inflammatory Bowel Disease Patients 长链非编码RNA-MALAT1和白细胞介素-6在炎症性肠病患者中的表达分析
4区 医学 Q4 ALLERGY Pub Date : 2023-11-07 DOI: 10.18502/ijaai.v22i5.13997
Mohsen Nemati Bajestan, Moein Piroozkhah, Vahid Chaleshi, Naser Elmi Ghiasi, Negar Jamshidi, Reza Mirfakhraie, Hedieh Balaii, Shabnam Shahrokh, Hamid Asadzadeh Aghdaei, Zahra Salehi, Ehsan Nazemalhosseini Mojarad
Inflammatory bowel disease (IBD) manifests as chronic inflammation within the gastrointestinal tract. The study focuses on a long noncoding RNA (lncRNA) known as Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). MALAT1's misregulation has been linked with various autoimmune diseases and regulates proinflammatory cytokines. The role of IL6 in immune-triggered conditions, including IBD, is another focal point. In this research, the expression of MALAT1 and IL6 in IBD patients was meticulously analyzed to uncover potential interactions. The study involved 33 IBD patients (13 with Crohn's disease and 20 with ulcerative colitis) and 20 healthy counterparts. Quantitative real-time polymerase chain reaction determined the MALAT1 and IL6 gene expression levels. The competitive endogenous RNA (ceRNA) regulatory network was constructed using several tools, including LncRRIsearch and Cytoscape. A deep dive into the Inflammatory Bowel Disease database was undertaken to understand IL6's role in IBD. Drugs potentially targeting these genes were also pinpointed using DGIdb. Results indicated a notable elevation in the expression levels of MALAT1 and IL6 in IBD patients versus healthy controls. MALAT1 and IL6 did not show a direct linear correlation, but IL6 could serve as MALAT1's target. Analyses unveiled interactions between MALAT1 and IL6, regulated by hsa-miR-202-3p, hsa-miR-1-3p, and has-miR-9-5p. IL6's pivotal role in IBD-associated inflammation, likely interacting with other cytokines, was accentuated. Moreover, potential drugs like CILOBRADINE for MALAT1 and SILTUXIMAB for IL6 were identified. This research underscored MALAT1 and IL6's potential value as targets in diagnosis and treatment for IBD patients.
炎症性肠病(IBD)表现为胃肠道的慢性炎症。这项研究的重点是一种名为转移相关肺腺癌转录本1 (MALAT1)的长链非编码RNA (lncRNA)。MALAT1的失调与多种自身免疫性疾病有关,并调节促炎细胞因子。il - 6在包括IBD在内的免疫触发性疾病中的作用是另一个焦点。本研究仔细分析了IBD患者中MALAT1和IL6的表达,以揭示潜在的相互作用。 该研究涉及33名IBD患者(13名患有克罗恩病,20名患有溃疡性结肠炎)和20名健康对照者。实时定量聚合酶链反应测定MALAT1和IL6基因表达水平。利用LncRRIsearch和Cytoscape等工具构建了竞争性内源性RNA (ceRNA)调控网络。深入研究炎症性肠病数据库以了解il - 6在IBD中的作用。潜在靶向这些基因的药物也通过ddgidb被确定。结果显示,与健康对照组相比,IBD患者的MALAT1和IL6表达水平显著升高。MALAT1与IL6没有直接的线性相关,但IL6 可以作为MALAT1的目标。分析揭示了MALAT1和IL6之间的相互作用,由hsa-miR-202-3p、hsa-miR-1-3p和has-miR-9-5p调节。IL6在ibd相关炎症中的关键作用,可能与其他细胞因子相互作用,被强调。此外,还发现了治疗MALAT1的CILOBRADINE和治疗IL6的SILTUXIMAB等潜在药物。 本研究强调了MALAT1和IL6作为IBD患者诊断和治疗靶点的潜在价值。
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引用次数: 0
Chronic Allergen Exposure Contributes to Steroid Resistance via Increased Phosphorylation of Glucocorticoid Receptors S226 and p38 MAPK in a Mouse Model of Asthma 在哮喘小鼠模型中,慢性过敏原暴露通过糖皮质激素受体S226和p38 MAPK磷酸化的增加有助于类固醇抵抗
4区 医学 Q4 ALLERGY Pub Date : 2023-11-07 DOI: 10.18502/ijaai.v22i5.13992
Yan Zhou, Limin Wang, Weizhong Jin, Chenhui Qiu, Hualiang Jin
Chronic allergen exposure can significantly induce p38 mitogen-activated protein kinase (MAPK) activation in asthma. p38 MAPK is involved in steroid resistance through phosphorylation of glucocorticoid receptors (GR) at S226. This study aims to investigate whether chronic allergen exposure can induce steroid resistance and whether it is associated with p38 MAPK activation in asthma. A mouse model of asthma was prepared by sensitizing and challenging mice with chronic ovalbumin (OVA) exposure. Key features of allergic asthma, encompassing bronchial hyperresponsiveness, pathology of lung tissues, cytokine profiles of inflammation in bronchoalveolar lavage fluid (BALF), and serum immunoglobulin (Ig)E concentration were evaluated. Furthermore, suppressive effects of corticosteroid on the splenocytes under stimulation of lipopolysaccharides, glucocorticoid receptor (GR) DNA binding ability of splenocytes, expression of GRα and phosphorylation of GR s226 in splenocytes, and p38 MAPK phosphorylation in splenocytes and lung tissues were determined. Chronic OVA exposure substantially induced airway hypersensitivity, leading to increased inflammatory infiltration in lung tissues. Additionally, it resulted in elevated levels of interleukin (IL)-4, IL-5, and IL-6 in BALF, as well as heightened levels of IgE in serum. Furthermore, OVA exposure substantially enhanced p38 MAPK phosphorylation in lung tissues. It also weakened the suppressive impacts of corticosteroids on splenocytes, impaired the GR DNA binding ability, and led to an enhanced phosphorylated state of GR S226 and p38 MAPK in splenocytes. Taken together, chronic allergen exposure contributes to steroid resistance in asthma, which is linked to an increased phosphorylated state of GR S226 and p38 MAPK.
慢性过敏原暴露可显著诱导哮喘患者p38丝裂原活化蛋白激酶(MAPK)的激活。p38 MAPK通过糖皮质激素受体(GR) S226位点的磷酸化参与类固醇抗性。本研究旨在探讨慢性过敏原暴露是否可诱导类固醇抵抗,以及是否与哮喘患者p38 MAPK激活有关。 通过致敏和激发慢性卵清蛋白暴露小鼠制备哮喘模型。我们评估了过敏性哮喘的主要特征,包括支气管高反应性、肺组织病理学、支气管肺泡灌洗液(BALF)炎症的细胞因子谱和血清免疫球蛋白(Ig)E浓度。进一步观察糖皮质激素对脂多糖刺激下脾细胞的抑制作用、脾细胞糖皮质激素受体(GR) DNA结合能力、脾细胞中GRα的表达和GR s226的磷酸化,以及脾细胞和肺组织中p38 MAPK的磷酸化。 长期暴露于OVA可显著诱导气道过敏,导致肺组织炎症浸润增加。此外,它导致BALF中白细胞介素(IL)-4、IL-5和IL-6水平升高,血清中IgE水平升高。此外,暴露于OVA可显著增强肺组织中p38 MAPK的磷酸化。它还削弱了皮质类固醇对脾细胞的抑制作用,损害了GR DNA的结合能力,导致脾细胞中GR S226和p38 MAPK的磷酸化状态增强。 综上所述,慢性过敏原暴露有助于哮喘中的类固醇抵抗,这与GR S226和p38 MAPK磷酸化状态的增加有关。
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引用次数: 0
PD-1/PD-L1 Interaction Regulates BCL2, KI67, BAX, and CASP3, Altering Proliferation, Survival, and Apoptosis in Acute Myeloid Leukemia PD-1/PD-L1相互作用调节BCL2、KI67、BAX和CASP3,改变急性髓性白血病的增殖、存活和凋亡
4区 医学 Q4 ALLERGY Pub Date : 2023-11-07 DOI: 10.18502/ijaai.v22i5.13998
Mojdeh Soltani, Mahshid Vosoughi, Mazdak Ganjalikhani-Hakemi, Hoorieh Shapoorian, Pezhman Beshkar, Nahid Eskandari, Behrooz Ghezelbash
Programmed death ligand‑1 (PD‑L1) is a pivotal inhibitory checkpoint ligand known to induce T-cell exhaustion via interaction with the programmed death‑1 (PD‑1) receptor. Beyond this, PD-L1’s intrinsic signaling pathways within cancer cells warrant further exploration. This study aims to elucidate the effect of PD-L1 stimulation on the proliferation, survival, and apoptosis of acute myeloid leukemia (AML) cell lines. Two human AML cell lines, HL-60 and THP-1 were cultured and treated with phorbol 12-myristate 13-acetate (PMA) to induce PD-L1overexpression. Post-treatment PD-L1 expression was confirmed via flow cytometry. Subsequently, cell surface PD-L1 was stimulated using a recombinant PD-1, 24 hours post-PMA treatment. The expression alterations in pivotal genes including BCL2, MKI67, BAX, and CASP3 were monitored using quantitative real-time polymerase chain reaction 24 and 48 hours post-treatment. Additionally, annexin-V through flow cytometry. Findings reveal that PD-L1 stimulation augments AML cell proliferation and survival by enhancing MKI67 and BCL2 expressions while concurrently inhibiting cell apoptosis due to decreased BAX and CASP3 expression following PD-L1 stimulation. Notably, stimulated cells expressed exhibited reduced annexin-V compared to control cells. This study underscores that PD-L1 stimulation fosters AML cell proliferation and survival while impeding cell apoptosis. The results hold potential implications for targeting PD-L1 in AML treatment strategies.
程序性死亡配体- 1 (PD - L1)是一种关键的抑制检查点配体,已知通过与程序性死亡- 1 (PD - 1)受体相互作用诱导t细胞衰竭。除此之外,PD-L1在癌细胞内的内在信号通路值得进一步探索。本研究旨在阐明PD-L1刺激对急性髓性白血病(AML)细胞系增殖、存活和凋亡的影响。培养2株人AML细胞株HL-60和THP-1,用PMA诱导pd - l1过表达。流式细胞术检测PD-L1表达。随后,在pma处理24小时后,用重组PD-1刺激细胞表面PD-L1。在治疗后24和48小时,采用实时定量聚合酶链反应监测关键基因BCL2、MKI67、BAX和CASP3的表达变化。此外,通过流式细胞术检测annexin-V。 研究结果表明,PD-L1刺激通过增强MKI67和BCL2的表达来增强AML细胞的增殖和存活,同时由于PD-L1刺激后BAX和CASP3的表达降低而抑制细胞凋亡。值得注意的是,与对照细胞相比,受刺激细胞表达的annexin-V减少。 这项研究强调,PD-L1刺激促进AML细胞增殖和存活,同时阻碍细胞凋亡。这些结果对靶向PD-L1的AML治疗策略具有潜在的意义。
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引用次数: 0
The Effect of Oral Montelukast in Controlling Asthma Attacks in Children; A Randomized Double-blind Placebo Control Study 口服孟鲁司特对儿童哮喘发作的控制作用随机双盲安慰剂对照研究
4区 医学 Q4 ALLERGY Pub Date : 2023-11-07 DOI: 10.18502/ijaai.v22i5.13990
Mohsen Jafari, Masoomeh Sobhani, Kambiz Eftekhari, Armen Malekiantaghi, Mohammad Gharagozlou, Alireza Shafiei
Oral Montelukast is recommended as maintenance therapy for persistent asthma, but there is controversy regarding its effectiveness in controlling asthma attacks. The present study was conducted to investigate the clinical efficacy of oral Montelukast for asthma attacks in children. This study was conducted as a double-blind placebo-controlled clinical trial on 80 children aged 1-14 years with asthma who were admitted to the emergency department of Bahrami Children's Hospital (Tehran, Iran) during one year. Patients were randomly divided into case and control groups. In addition to the standard asthma attack treatment, Montelukast was prescribed in the case group and placebo in the control group for one week. Patients were evaluated in terms of asthma attack severity score and oxygen saturation percentage (SpO2) in room air as primary outcomes 1, 4, 8, 24 and 48 hours after admission. In the first 48 hours, there was no significant difference in the score of asthma attack severity and SpO2 between the case and control groups. There was no significant difference between the groups in terms of length of hospitalization or number of admissions to the intensive care unit. None of the patients were re-hospitalized after discharge. The results of this study showed that the use of Montelukast along with the standard treatment of asthma attacks in children has no added benefit.
口服孟鲁司特被推荐作为持续性哮喘的维持治疗,但其控制哮喘发作的有效性存在争议。本研究旨在探讨口服孟鲁司特治疗儿童哮喘发作的临床疗效。 本研究是一项双盲安慰剂对照临床试验,研究对象是在伊朗德黑兰Bahrami儿童医院急诊科住院一年的80名1-14岁哮喘患儿。患者随机分为病例组和对照组。除了标准的哮喘发作治疗外,病例组使用孟鲁司特,对照组使用安慰剂,疗程为一周。入院后1、4、8、24和48小时,以哮喘发作严重程度评分和室内空气氧饱和度百分比(SpO2)作为主要结局对患者进行评估。治疗前48小时,病例组与对照组哮喘发作严重程度评分和SpO2评分差异无统计学意义。在住院时间和入住重症监护病房的人数方面,两组之间没有显著差异。出院后无患者再次住院。 这项研究的结果表明,使用孟鲁司特与标准治疗哮喘发作的儿童没有额外的好处。
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引用次数: 0
Role of Long Non-coding RNA HSD17B3-AS1 in Trauma for COVID-19. 长非编码RNA HSD17B3-AS1在新冠肺炎创伤中的作用。
IF 1.2 4区 医学 Q4 ALLERGY Pub Date : 2023-09-03 DOI: 10.18502/ijaai.v22i4.13607
Amir-Reza Javanmard, Hadi Esmaeili Gouvarchinghaleh, Ruhollah Dorostkar, Mahdi Tat

COVID-19, an acute respiratory syndrome caused by the SARS-CoV-2 virus, was first reported in late 2019 in Wuhan, China, and rapidly escalated into a global pandemic. The condition can lead to organ dysfunction and ultimately death through its onset of acute respiratory distress syndrome (ARDS). Disease severity has been linked to proinflammatory cytokines which activate the NF-κB and STAT transcription factors in infected cells. It has been proven that lncRNAs play a very important role in reducing or increasing inflammatory factors. This makes them potentially valuable in recognizing pathogenesis pathways and therapeutic targets in COVID-19. Nanocurcumin is known as an antioxidant, tumor suppressor and anti-inflammatory substance, and it can be effective to reduce inflammation caused by the disease of COVID-19. This study analyzed Sequence Read Archive data from COVID-19 patients with acute versus milder symptoms, identifying dysregulated genes and non-coding RNAs. To verify this correlation, the expression of the candidate gene was evaluated with quantitative polymerase chain reaction (qPCR) in mouse models, while immunoglobulin (Ig) G titer was measured using enzyme-linked immunosorbent assay (ELISA) in mouse serum samples. Here we introduced a novel lncRNA called HSD17B3-AS1, suggested as a therapeutic target in COVID-19 patients with acute symptoms. Furthermore, we revealed nanocurcumin is reducing the expression of HSD17B3-AS1 which leads to reduced inflammation in mice. These results suggest that HSD17B3-AS1 plays a significant regulatory role in managing COVID-19, and the downregulation of HSD17B3-AS1 by Nanocurcumin presents a promising treatment option for minimizing complications in COVID-19 patients.

新冠肺炎是一种由SARS-CoV-2病毒引起的急性呼吸综合征,于2019年末在中国武汉首次报告,并迅速升级为全球大流行。这种情况可导致器官功能障碍,并最终因急性呼吸窘迫综合征(ARDS)发作而死亡。疾病的严重程度与促炎细胞因子有关,这些细胞因子激活受感染细胞中的NF-κB和STAT转录因子。已经证明lncRNA在减少或增加炎症因子方面发挥着非常重要的作用。这使得它们在识别新冠肺炎的发病途径和治疗靶点方面具有潜在的价值。纳米姜黄素是一种抗氧化、抑瘤和抗炎物质,可有效减少新冠肺炎引起的炎症。这项研究分析了新冠肺炎急性和轻度症状患者的序列读取档案数据,确定了失调基因和非编码RNA。为了验证这种相关性,在小鼠模型中用定量聚合酶链式反应(qPCR)评估候选基因的表达,而在小鼠血清样本中用酶联免疫吸附试验(ELISA)测量免疫球蛋白(Ig)G滴度。在这里,我们介绍了一种新的lncRNA,称为HSD17B3-AS1,被建议作为新冠肺炎急性症状患者的治疗靶点。此外,我们发现纳米姜黄素降低了HSD17B3-AS1的表达,从而减少了小鼠的炎症。这些结果表明,HSD17B3-AS1在管理新冠肺炎中发挥着重要的调节作用,纳米姜黄素对HSD17B3-AS1的下调为新冠肺炎患者减少并发症提供了一种有前景的治疗选择。
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引用次数: 0
The Radiological Manifestations of Phagocytic Primary Immunodeficiencies in Children. 儿童吞噬细胞原发性免疫缺陷的放射学表现。
IF 1.5 4区 医学 Q4 ALLERGY Pub Date : 2023-09-03 DOI: 10.18502/ijaai.v22i4.13612
Mitra Khalili, Zahra Chavoshzadeh, Sepideh Darougar, Mahboubeh Mansouri, Narges Eslami, Delara Babaie, Mehrnaz Mesdaghi, Abdollah Karimi, Shahnaz Armin, Alireza Fahimzad, Roxana Mansour Ghanaei, Sedigheh Rafiee Tabatabaie, Fatemeh Akrami

Primary immunodeficiencies are a diverse group of rare genetic disorders, among which phagocytic dysfunction impairs neutrophil function in a wide range of inherited disorders. Due to the heterogeneity of the disorders a multidisciplinary approach is often required for early diagnosis and initiation of appropriate treatments. The aim of this study was to evaluate the imaging findings in children admitted with phagocytic primary immunodeficiencies. Thirty-five children who fulfilled the inclusion criteria for phagocytic dysfunction were enrolled in this study. The patients were under close observation and monitoring from January 2011 until data locking in December 2017. The diagnosis of phagocytic immunodeficiency was confirmed by the patient's clinical course, presentation features, and laboratory data.  Among the 35 patients studied, the most frequent condition was chronic granulomatous disease (CGD) (23 patients), followed by different types of neutropenia (8 patients) and Job's syndrome (4 patients). Mediastinal and hilar lymphadenopathies and consolidation were the most frequent presentations. There was a significant relationship between mediastinal/hilar lymphadenopathies and fungal infections. A meaningful relationship was also found between pulmonary nodules without halo signs in patients with concomitant tuberculosis and fungal infections. A significant correlation was found between CGD, pulmonary fibrotic changes, and mediastinal lymphadenopathies. The most frequent radiological manifestations in children included mediastinal and hilar consolidations. Physicians' awareness of the radiological and clinical manifestations of these inherited diseases may be helpful in the early diagnosis and timely initiation of specific prophylaxis measures to prevent infections and also to initiate hematopoietic stem cell transplantation as the curative management modality.

原发性免疫缺陷是一组罕见的遗传性疾病,其中吞噬功能障碍损害了多种遗传性疾病中的中性粒细胞功能。由于疾病的异质性,通常需要多学科的方法来进行早期诊断和开始适当的治疗。本研究的目的是评估因吞噬细胞原发性免疫缺陷而入院的儿童的影像学表现。35名符合吞噬功能障碍纳入标准的儿童被纳入本研究。从2011年1月到2017年12月数据锁定,患者一直处于密切观察和监测之下。吞噬细胞免疫缺陷的诊断通过患者的临床病程、表现特征和实验室数据得到证实。在研究的35名患者中,最常见的情况是慢性肉芽肿性疾病(CGD)(23名患者),其次是不同类型的中性粒细胞减少症(8名患者)和乔布斯综合征(4名患者)。纵隔和肺门淋巴结病和巩固是最常见的表现。纵隔/肺门淋巴结病与真菌感染之间存在显著关系。在伴有结核病和真菌感染的患者中,没有晕染迹象的肺结节之间也发现了有意义的关系。CGD、肺纤维化改变和纵隔淋巴结病之间存在显著相关性。儿童最常见的放射学表现包括纵隔和肺门实变。医生对这些遗传性疾病的放射学和临床表现的认识可能有助于早期诊断和及时采取具体的预防措施来预防感染,也有助于启动造血干细胞移植作为治疗管理模式。
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引用次数: 0
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Iranian journal of allergy, asthma, and immunology
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