• 文章类型: Journal Article
    背景:食物蛋白诱导的小肠结肠炎综合征(FPIES)是一种非IgE介导的食物过敏,其特征是在触发食物摄入后1-4小时内出现胃肠道症状。在文学中,一些作者先前已经描述了FPIES患者可能对相同的触发食物产生IgE介导的过敏的可能性,尤其是牛奶(CM)。病例介绍:我们报告了5例CM-FPIES转化为IgE介导的CM变态反应在我们的三级儿科变态反应单位,并进行了文献综述,旨在表征有发生这种转变风险的患者的临床特征。结论:这种现象提出了一个问题,即IgE介导的和非IgE介导的过敏是否代表相同的疾病谱,并强调需要进一步研究以了解该过程的病理生理机制。
    Background: Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated food allergy characterized by gastrointestinal symptom onset within 1-4 hours from trigger food ingestion. In the literature, some authors have previously described the possibility that a patient with FPIES may develop an IgE-mediated allergy to the same trigger food, especially cow\'s milk (CM). Case Presentation: We reported five cases of CM-FPIES converting to IgE-mediated CM allergy presented at our tertiary pediatric Allergy Unit and performed a review of the literature, aiming to characterize the clinical features of patients who are at risk of developing such conversion. Conclusions: This phenomenon raises the question of whether IgE-mediated and non-IgE-mediated allergies represent a spectrum of the same disease and highlights the need for further investigation to understand the pathophysiological mechanisms of this process.
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  • 文章类型: Journal Article
    无伴随荨麻疹的血管性水肿是重组组织型纤溶酶原激活剂(r-tPA)阿替普酶及其基因修饰变体替奈普酶治疗的众所周知的并发症。当引起气道阻塞时,它可能是致命的,并且可能需要插管。美国心脏协会/美国卒中协会关于急性缺血性卒中患者早期治疗的最新指南建议首先通过干扰组胺途径来治疗这种并发症。本文旨在阐明r-tPA诱导的血管性水肿的病理生理机制,并提供了几种论点,即这种情况主要是缓激肽介导的,因此应首先通过缓激肽途径进行干预来治疗。第二,本文还描述了r-tPA治疗后其他较少报道的不良症状及其导致特异性治疗的病理生理机制.该手稿描述了需要更新美国心脏协会/美国中风协会指南中的“3.5IV阿替普酶”部分,以充分治疗这种r-tPA诱导的血管性水肿并防止潜在的致命后果。
    Angioedema without concomitant urticaria is a well-known complication of treatment with the recombinant tissue-type plasminogen activator (r-tPA) alteplase and its genetically modified variant tenecteplase. It is potentially lethal when causing airway obstruction and can require intubation. The latest guideline for the early management of patients with acute ischemic stroke from the American Heart Association/American Stroke Association advises to treat this complication initially by interfering with the histamine pathway. This article aims to clarify the pathophysiological mechanism of r-tPA-induced angioedema and provides several arguments that this condition is primarily bradykinin-mediated and hence should be treated initially by intervening with the bradykinin pathway. Second, other-less frequently reported-adverse symptoms after r-tPA therapy and their proposed pathophysiological mechanisms leading to specific treatment are described. This manuscript describes the need for an update of the section \"3.5 IV alteplase\" from the American Heart Association/American Stroke Association guideline to treat this r-tPA-induced angioedema adequately and prevent potentially fatal outcomes.
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  • 文章类型: Journal Article
    暂无摘要。
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  • 文章类型: Journal Article
    固有淋巴细胞(ILC)和适应性T淋巴细胞促进组织稳态和保护性免疫反应。它们的产生取决于转录因子GATA3,该转录因子在ILC2s和T辅助细胞中进一步升高,以在组织修复期间驱动2型免疫,过敏性疾病,和抗蠕虫免疫力.对这种关键的上调的控制知之甚少。在ILC中使用CRISPR筛选,我们鉴定了以前未被理解的心肌细胞特异性增强因子2d(Mef2d)介导的GATA3依赖性2型淋巴细胞分化的调节。来自ILC2s和/或T细胞的Mef2d缺失特异性保护免受过敏原肺攻击。Mef2d抑制Regnase-1内切核酸酶的表达以增强IL-33受体的产生和IL-33信号传导,并在钙介导的信号传导的下游起作用,使NFAT1易位到细胞核以促进2型细胞因子介导的免疫。
    Innate lymphoid cells (ILCs) and adaptive T lymphocytes promote tissue homeostasis and protective immune responses. Their production depends on the transcription factor GATA3, which is further elevated specifically in ILC2s and T helper 2 cells to drive type-2 immunity during tissue repair, allergic disorders, and anti-helminth immunity. The control of this crucial up-regulation is poorly understood. Using CRISPR screens in ILCs we identified previously unappreciated myocyte-specific enhancer factor 2d (Mef2d)-mediated regulation of GATA3-dependent type-2 lymphocyte differentiation. Mef2d-deletion from ILC2s and/or T cells specifically protected against an allergen lung challenge. Mef2d repressed Regnase-1 endonuclease expression to enhance IL-33 receptor production and IL-33 signaling and acted downstream of calcium-mediated signaling to translocate NFAT1 to the nucleus to promote type-2 cytokine-mediated immunity.
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  • 文章类型: Journal Article
    据报道,土地利用和气候变化的变化会减少环境和人类微生物群的生物多样性。生物多样性的这些减少可能导致免疫调节回路的刺激不足和不平衡,最终,临床疾病,比如哮喘和过敏。
    我们总结了关于内在(肠道,皮肤,和气道)和外部(空气,土壤,天然水域,植物,和动物)哮喘发展过程中的生物多样性层,喘息,和过敏致敏。
    我们在SciVerseScopus进行了系统的搜索,PubMedMEDLINE,和WebofScience直到2024年3月5日,以确定相关的人类研究,评估生物多样性的内部和外部层与哮喘风险之间的关系,喘息,或过敏致敏。该协议在PROSPERO(CRD42022381725)中注册。
    总共筛选了2,419项研究,在排除和447项研究的全文回顾之后,82项研究被纳入综合研究,最后审查。29项研究报道了外层生物多样性在哮喘发展中的保护作用,喘息,或过敏致敏。还有16项研究表明外层生物多样性对增加哮喘的影响,喘息,或过敏致敏。然而,没有明确的证据表明内层生物多样性在哮喘发展中的作用,喘息,和过敏性致敏(13项研究报告了保护作用,15项研究报告了风险增加的证据).
    根据文献综述,未来的系统评价可以更具体地关注外层生物多样性和哮喘.与内层生物多样性的关联不太可能有足够的证据进行系统审查。基于这一全面审查,有必要进行基于人群的纵向研究,以确定生命过程中进入成年期的关键暴露期,并更好地了解将环境暴露与微生物组组成变化联系起来的机制,多样性,和/或功能发展为哮喘和过敏性致敏。https://doi.org/10.1289/EHP13948.
    UNASSIGNED: Changes in land use and climate change have been reported to reduce biodiversity of both the environment and human microbiota. These reductions in biodiversity may lead to inadequate and unbalanced stimulation of immunoregulatory circuits and, ultimately, to clinical diseases, such as asthma and allergies.
    UNASSIGNED: We summarized available empirical evidence on the role of inner (gut, skin, and airways) and outer (air, soil, natural waters, plants, and animals) layers of biodiversity in the development of asthma, wheezing, and allergic sensitization.
    UNASSIGNED: We conducted a systematic search in SciVerse Scopus, PubMed MEDLINE, and Web of Science up to 5 March 2024 to identify relevant human studies assessing the relationships between inner and outer layers of biodiversity and the risk of asthma, wheezing, or allergic sensitization. The protocol was registered in PROSPERO (CRD42022381725).
    UNASSIGNED: A total of 2,419 studies were screened and, after exclusions and a full-text review of 447 studies, 82 studies were included in the comprehensive, final review. Twenty-nine studies reported a protective effect of outer layer biodiversity in the development of asthma, wheezing, or allergic sensitization. There were also 16 studies suggesting an effect of outer layer biodiversity on increasing asthma, wheezing, or allergic sensitization. However, there was no clear evidence on the role of inner layer biodiversity in the development of asthma, wheezing, and allergic sensitization (13 studies reported a protective effect and 15 reported evidence of an increased risk).
    UNASSIGNED: Based on the reviewed literature, a future systematic review could focus more specifically on outer layer biodiversity and asthma. It is unlikely that association with inner layer biodiversity would have enough evidence for systematic review. Based on this comprehensive review, there is a need for population-based longitudinal studies to identify critical periods of exposure in the life course into adulthood and to better understand mechanisms linking environmental exposures and changes in microbiome composition, diversity, and/or function to development of asthma and allergic sensitization. https://doi.org/10.1289/EHP13948.
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  • 文章类型: Case Reports
    Alpha-gal过敏或红肉过敏是一种罕见但可能严重的过敏。在蜱虫叮咬过程中,当存在于蜱虫唾液中的α-gal转移到人类时,通常会发生敏化,促使产生针对α-gal的IgE抗体。随后接触含有α-gal的哺乳动物肉或其他产品可导致过敏反应。
    一名60多岁的健康男子因急性过敏反应入院。多次蜱叮咬和最近食用哺乳动物肉的历史引起了人们对α-gal综合征引起的过敏反应的怀疑。
    α-gal综合征的诊断是基于升高的α-galIgE抗体,并得到病史和临床评估的进一步支持。他出院时的饮食指示是消除含有alpha-gal的食物和产品,并根据当地指南管理过敏症状和过敏反应。
    UNASSIGNED: Alpha-gal allergy or red meat allergy is a rare yet potentially severe allergy. Sensitisation usually occurs when alpha-gal present in the tick\'s saliva is transferred to humans during a tick bite, prompting the production of IgE antibodies to alpha-gal. Subsequent exposure to mammalian meat or other products containing alpha-gal can lead to allergic reactions.
    UNASSIGNED: A previously healthy man in his sixties was admitted with acute anaphylaxis. A history of multiple tick bites and recent consumption of mammalian meat raised suspicion of anaphylaxis caused by alpha-gal syndrome.
    UNASSIGNED: A diagnosis of alpha-gal syndrome was given based on elevated alpha-gal IgE antibodies, and further supported by medical history and clinical assessment. He was discharged with dietary instructions to eliminate food and products containing alpha-gal, and to manage allergy symptoms and anaphylaxis according to local guidelines.
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  • 文章类型: Case Reports
    UNASSIGNED: Identify countries that have legislation on mandatory declarations of food allergens, irradiated foods, and transgenic foods on the nutritional labels of packaged foods.
    UNASSIGNED: Exploratory study reviewing the health regulations and technical standards for foods in Latin American countries in order to gather information on declarations of allergens, trace allergens, irradiated foods, and transgenic foods. The information search was carried out through the countries\' government web pages. Presentation of the results is descriptive and narrative.
    UNASSIGNED: Of the 19 countries reviewed, 89% require a declaration of allergens on their nutrition labeling, 76% have legislation that explicitly require a statement on trace allergens, and 82% follow Codex Alimentarius recommendations with some modifications of food categories.
    UNASSIGNED: Three pending challenges in the Region are: requiring statements on allergens as a food safety measure; making progress toward improved labeling of trace allergens; and ensuring universal availability of epinephrine.
    UNASSIGNED: Identificar os países que têm legislação relacionada à declaração obrigatória de alimentos alergênicos, irradiados e transgênicos na rotulagem nutricional de alimentos embalados.
    UNASSIGNED: Estudo exploratório com revisão dos regulamentos sanitários ou normas técnicas de alimentos dos países da América Latina, a fim de coletar informações sobre a declaração de alimentos alergênicos, traços de alergênicos, alimentos irradiados e transgênicos na rotulagem nutricional. A busca de informações foi realizada por meio dos sites governamentais dos países. Os resultados são apresentados de forma descritiva e narrativa.
    UNASSIGNED: Dos 19 países analisados, 89% declaram alergênicos na rotulagem nutricional, 76% incorporam explicitamente a declaração de traços na legislação e 82% seguem as recomendações do Codex Alimentarius, com algumas modificações nas categorias de alimentos.
    UNASSIGNED: Entre os desafios pendentes na Região estão a implementação da declaração de alergênicos como medida de segurança alimentar e a melhoria da rotulagem de traços de alergênicos e da disponibilidade universal de epinefrina.
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  • 文章类型: Journal Article
    过敏性致敏是桦树花粉(BP)过敏性气道炎症发展的重要步骤;然而,这个过程还有待充分阐明。最近的科学进展强调了过敏原背景的重要性。在这方面,BP上存在的微生物模式(PAMPs)引起了越来越多的兴趣。由于这些PAMP被专门的模式识别受体(PRR)识别,本研究旨在探讨细胞内PRRs和炎性小体调节因子NLRP3的作用。
    我们建立了生理相关的鼻内和无佐剂致敏程序来研究BP诱导的全身和局部肺部炎症。
    引人注目的是,BP致敏的Nlrp3缺陷小鼠显示出显著较低的IgE水平,Th2相关细胞因子,细胞浸润到肺中,粘蛋白产生和上皮增厚比他们的野生型对应物,这似乎与炎症小体的形成无关。有趣的是,骨髓嵌合体显示,NLRP3在造血系统中的表达是引发过敏反应所必需的.
    总的来说,这项研究确定NLRP3是BP诱导的过敏性免疫反应的重要驱动因素.
    UNASSIGNED: Allergic sensitization is an essential step in the development of allergic airway inflammation to birch pollen (BP); however, this process remains to be fully elucidated. Recent scientific advances have highlighted the importance of the allergen context. In this regard, microbial patterns (PAMPs) present on BP have attracted increasing interest. As these PAMPs are recognized by specialized pattern recognition receptors (PRRs), this study aims at investigating the roles of intracellular PRRs and the inflammasome regulator NLRP3.
    UNASSIGNED: We established a physiologically relevant intranasal and adjuvant-free sensitization procedure to study BP-induced systemic and local lung inflammation.
    UNASSIGNED: Strikingly, BP-sensitized Nlrp3-deficient mice showed significantly lower IgE levels, Th2-associated cytokines, cell infiltration into the lung, mucin production and epithelial thickening than their wild-type counterparts, which appears to be independent of inflammasome formation. Intriguingly, bone-marrow chimera revealed that expression of NLRP3 in the hematopoietic system is required to trigger an allergic response.
    UNASSIGNED: Overall, this study identifies NLRP3 as an important driver of BP-induced allergic immune responses.
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  • 文章类型: Journal Article
    近几十年来,儿童过敏性疾病的患病率急剧增加。这些情况显著影响过敏儿童及其家庭的生活质量。乳铁蛋白,在各种生物液体中发现的多功能糖蛋白,正在成为一种有前途的免疫调节剂,可以潜在地缓解儿童的过敏性疾病。乳铁蛋白的多方面特性使其成为管理这些条件的令人信服的候选人。首先,乳铁蛋白表现出有效的抗炎和抗氧化活性,可以减轻过敏性疾病的慢性炎症特征。其次,它的铁结合能力可能有助于调节过敏儿童的铁平衡,可能影响他们症状的严重程度。乳铁蛋白还表现出抗菌性能,使其有益于预防通常与呼吸道过敏相关的继发感染。此外,其调节免疫反应和调节炎症途径的能力表明其作为免疫平衡剂的潜力。对当前文献的回顾强调需要进一步研究以阐明乳铁蛋白在过敏性疾病中的确切作用。利用乳铁蛋白的免疫调节潜力可以提供一种新的附加方法来管理儿童过敏性疾病,为改善结果和提高儿科患者及其家人的生活质量提供希望。随着乳铁蛋白继续引起研究人员的注意,它的特性和多样化的应用使它成为一个有趣的研究课题,具有丰富的历史和充满希望的未来。
    The prevalence of allergic diseases has dramatically increased among children in recent decades. These conditions significantly impact the quality of life of allergic children and their families. Lactoferrin, a multifunctional glycoprotein found in various biological fluids, is emerging as a promising immunomodulatory agent that can potentially alleviate allergic diseases in children. Lactoferrin\'s multifaceted properties make it a compelling candidate for managing these conditions. Firstly, lactoferrin exhibits potent anti-inflammatory and antioxidant activities, which can mitigate the chronic inflammation characteristic of allergic diseases. Secondly, its iron-binding capabilities may help regulate the iron balance in allergic children, potentially influencing the severity of their symptoms. Lactoferrin also demonstrates antimicrobial properties, making it beneficial in preventing secondary infections often associated with respiratory allergies. Furthermore, its ability to modulate the immune response and regulate inflammatory pathways suggests its potential as an immune-balancing agent. This review of the current literature emphasises the need for further research to elucidate the precise roles of lactoferrin in allergic diseases. Harnessing the immunomodulatory potential of lactoferrin could provide a novel add-on approach to managing allergic diseases in children, offering hope for improved outcomes and an enhanced quality of life for paediatric patients and their families. As lactoferrin continues to capture the attention of researchers, its properties and diverse applications make it an intriguing subject of study with a rich history and a promising future.
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  • 文章类型: Journal Article
    背景:筛查和治疗潜在结核病感染(LTBI)的医护人员(HCWs)对于控制结核病(TB)感染至关重要。抗结核药物的不良反应(ADR)对患者安全和治疗完成提出了挑战。目的:本研究探讨人类白细胞抗原(HLA)等位基因与ADR风险之间的关系。尤其是药物超敏反应(DHS)和肝毒性,在接受异烟肼(INH)和利福平(RIF)治疗的LTBIHCWs中。方法:本研究包括接受3个月INH和RIF方案的患有LTBI的韩国HCWs。对治疗期间出现ADR的HCWs进行HLA基因分型,以及对照组由未发生ADR的个体组成.结果:在67例患者中,29例(43.2%)在INH和RIF治疗期间出现不良反应。与对照组(DHS-/H-)相比,无肝毒性的DHS患者(DSH/H-)的HLA-A*11:01等位基因频率更高(4/9,44.4%vs.3/38,7.9%;奇数比率[OR],8.554;95%置信区间[CI],1.415-59.869;p=0.018)。相反,HLA-DPB1*05:01与肝毒性风险增加相关,无论DHS如何(10/20,50%vs.5/38,13.2%;或,5.323;95%CI,1.493-21.518;p=0.011)。在具有肝毒性的DHS组(DHS/H)中,HLA-DPB1*05:01的比例较高(3/5,60%vs.5/38,13.2%;或,8.912;95%CI,1.110-92.993;p=0.037),而在该组中未观察到HLA-A*11:01。结论:HLA-A*11:01等位基因与DHS风险增加相关,无肝脏毒性,而HLA-DPB1*05:01等位基因与肝毒性风险增加相关.
    Background: Screening and treating healthcare workers (HCWs) for latent tuberculosis infection (LTBI) are essential for tuberculosis (TB) infection control. Adverse drug reactions (ADRs) to anti-TB drugs present challenges to patient safety and treatment completion. Objective: This study investigated the association between human leukocyte antigen (HLA) alleles and the risk of ADRs, especially drug hypersensitivity (DHS) and hepatotoxicity, in HCWs with LTBI receiving isoniazid (INH) and rifampin (RIF) therapy. Methods: Korean HCWs with LTBI who received a 3 month INH and RIF regimen were included in this study. HLA genotyping was performed on HCWs who experienced ADRs during treatment, as well as the control group consisted of individuals who did not develop ADRs. Results: Of the 67 patients, 29 (43.2%) experienced ADRs during INH and RIF therapy. The HLA-A*11:01 allele was more frequent in patients with DHS without hepatotoxicity (DSH+/H-) compared to the control group (DHS-/H-) (4/9, 44.4% vs. 3/38, 7.9%; odd ratio [OR], 8.554; 95% confidence interval [CI], 1.415-59.869; p = 0.018). Conversely, HLA-DPB1*05:01 was associated with an increased risk of hepatotoxicity regardless of DHS (10/20, 50% vs. 5/38, 13.2%; OR, 5.323; 95% CI, 1.493-21.518; p = 0.011). In the DHS with hepatotoxicity group (DHS+/H+), HLA-DPB1*05:01 was present in a higher proportion (3/5, 60% vs. 5/38, 13.2%; OR, 8.912; 95% CI, 1.110-92.993; p = 0.037), whereas HLA-A*11:01 was not observed in this group. Conclusions: The HLA-A*11:01 allele was associated with an increased risk of DHS without hepatotoxicity, whereas the HLA-DPB1*05:01 allele was associated with an increased risk of hepatotoxicity.
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