蠕虫及其衍生物对过敏性疾病的抑制作用

蠕虫感染极为普遍,全球大约有1/4人口感染,世界各地均有分布,尤其是热带农村地区的流行率最高。蠕虫病主要表现为:嗜酸性粒细胞增多,血清抗体水平增高,速发型皮肤过敏反应等。但随着蠕虫与宿主长期协同演化,二者之间不再是一味的损伤,近些年来大量流行病学调查和动物实验研究显示:部分蠕虫及其衍生物能够抑制过敏性疾病的发生发展。本文就其免疫机制及几种蠕虫在过敏性疾病中作用的研究进行综述。     

肠道菌群与过敏性疾病

近年有关过敏性疾病的流行病学调查、粪便菌群分析和临床研究提示,过敏性疾病的发生与发展与早期肠道菌群的紊乱有密切的关联性。1过敏性疾病概述过敏性疾病(又称变态反应性疾病)被世界卫生组织(WHO)认为是当今世界性的重大卫生学问题。过敏性疾病主要包括变应性鼻炎、过敏性结     

生物素-亲和素及其应用(续三)——生物素-抗生物素蛋白微量ELISA检测人IgE

<正> 自从1966年Ishizaka在研究过敏性疾病时开拓性地发现IgE以来,学者们对IgE的研究发生了极大的兴趣,各种研究报告相继出现。 IgE又称反应素或亲细胞性抗体。与其他几类Ig相比,IgE在正常人血浆中含量极低,为0.01～0.9mg％,仅占血清蛋白总量的0.002％。但在各种变态反应性疾病如过敏性哮喘、枯草热、荨麻疹、过敏性鼻炎、药物过敏,某些感染性疾病和肿瘤如麻疯、天疱疮、何杰金氏病、IgE骨髓瘤以及某些细胞免疫缺陷等均可见IgE升高。在蠕虫感染     

呼吸道过敏性疾病与社会心理因素双向关系的Meta分析

目的：系统评价呼吸道过敏性疾病和社会心理因素的关系。方法：计算机检索Cochrance图书馆、Medline、EMbase、Pubmed、CBM、CNKI等数据库,查找包括心理社会因素对呼吸道过敏性疾病的影响或者呼吸道过敏性疾病对精神健康影响的临床研究。根据纳入和排除标准选择文献,对符合纳入标准的文献进行Meta分析,计算其合并OR值及95％CI。结果：共纳入20个病例研究（13篇文献）,其中13个研究评估心理社会因素对呼吸道过敏性疾病的影响,7个研究评估效果呼吸道过敏性疾病对心理健康的影响。在这些研究中呼吸道过敏性疾病是评估哮喘和过敏性鼻炎。Meta分析结果显示社会心理因素和呼吸道疾病的发生发展有关[OR=1．77,95％CI（1．42,2．22）],呼吸道过敏性疾病与未来不健康的心理发生发展有关[OR=1．73,95％CI（1．47,2．03）]。结论：当前的研究发现呼吸道过敏性疾病和社会心理因素有很大的关系。这支持在呼吸道过敏性疾病治疗除了传统的生理和药理干预外,心理干预呼吸道对过敏性疾病的预防和管理也发挥作用。     

肠道菌群与婴幼儿过敏性疾病

肠道菌群是一个被遗忘的"器官",其在宿主消化营养免疫发育等诸多方面发挥着极为重要的作用。0~3岁是婴幼儿肠道菌群建立的关键时间窗,其与肠道免疫系统的成熟同步,是形成免疫耐受的关键时期,如果这一时期肠道菌群发生紊乱,可导致免疫耐受破坏,引起婴幼儿过敏性疾病。近年来流行病学调查和实验研究提示婴幼儿早期肠道菌群紊乱与过敏性疾病的发生发展密切相关,本研究就婴幼儿常见过敏性疾病如特应性皮炎、食物过敏、哮喘、过敏性鼻炎等与肠道菌群的相关性进行综述。     

首届中国深圳临床微生态学国际高峰论坛(2010)通知

临床微生态学是运用微生态学理论和方法来研究人类菌群相关疾病的发生发展、诊断、治疗和预防的临床分支学科。近年来随着研究方法与技术的不断突破,临床微生态学的基础研究、临床研究取得重大进展：肠道菌群与炎症性肠病、功能性胃肠疾病、幽门螺杆菌感染、过敏性疾病、2型糖尿病、肥胖等疾病的关系成为临床研究热点。     

抗寄生虫分子疫苗的展望

<正>人们可以预料,预防性疫苗是免疫寄生虫学研究中有实践意义的主要成果。目前正在探索的疫苗是分子疫苗,分子疫苗是由一个或多个有足够长度、结构完整的寄生虫天然分子所组成。分子疫苗主要是预防蠕虫、原虫和节肢动物寄生虫的初次感染或继续感染,亦可预防寄生虫感染引起的严重疾病,其次是降低寄生虫种群在敏感宿主中间的传播率。     

呼吸道过敏性疾病与社会心理因素双向关系的Meta分析

目的:系统评价呼吸道过敏性疾病和社会心理因素的关系。方法:计算机检索Cochrance图书馆、Medline、EMbase、Pubmed、CBM、CNKI等数据库,查找包括心理社会因素对呼吸道过敏性疾病的影响或者呼吸道过敏性疾病对精神健康影响的临床研究,根据纳入和排除标准选择文献,对符合纳入标准的文献进行Meta分析,计算其合并OR值及95%CI。结果:共纳入20个病例研究(13篇文献),其中13个研究评估心理社会因素对呼吸道过敏性疾病的影响,7个研究评估效果呼吸道过敏性疾病对心理健康的影响。在这些研究中呼吸道过敏性疾病是评估哮喘和过敏性鼻炎。Meta分析结果显示社会心理因素和呼吸道疾病的发生发展有关[OR=1.77,95%CI(1.42,2.22)],呼吸道过敏性疾病与未来不健康的心理发生发展有关[OR=1.73,95%CI(1.47,2.03)]。结论:当前的研究发现呼吸道过敏性疾病和社会心理因素有很大的关系。这支持在呼吸道过敏性疾病治疗除了传统的生理和药理干预外,心理干预呼吸道对过敏性疾病的预防和管理也发挥作用。     

盐城地区未成年过敏性疾病患者吸入性过敏原IgE检测结果分析

摘要 目的：通过研究分析盐城地区未成年过敏性疾病患者吸入性过敏原特异性IgE检测结果分布变化特点,为过敏性疾病预防和临床诊疗提供科学依据。方法：自2020年1月至2021年3月期间,选择430例未成年(<18岁)过敏性疾病患者,血清检测方法采用欧蒙公司生产的过敏原特异性IgE检测试剂盒。结果：430例患者中,血清过敏原IgE阳性166例(38.60%),其中尘螨和屋尘是主要的吸入性过敏原。血清IgE阳性率男性39%,女性36% (P>0.05),中学组女性阳性率（61.11 %）高于男性（45.83 %）（P<0.05）。不同年龄组间IgE阳性率有统计学差异（P<0.05）,蟑螂、尘螨、霉菌、豚草、屋尘和年龄组间有统计学差异（P<0.05）。不同临床症状与IgE阳性率有统计学差异(P<0.05),其中呼吸道过敏症状组IgE阳性率最高（48.30 %）,不同症状组间主要过敏原都是尘螨。屋尘阳性患者均合并尘螨阳性,其中70.93 %的患者表现出了呼吸道过敏症状。结论：尘螨、屋尘是盐城地区未成年过敏性疾病患者最主要的吸入性过敏原,研究血清过敏原分布,对未成年人过敏性疾病的预防、诊疗具有重要意义。     

益生菌防治过敏性疾病的进展和展望

过敏是一种病理性的免疫反应。随着全球患病率逐年上升,它已成为困扰人类健康的常见疾病。目前针对过敏性疾病的疗法大都收效甚微。研究证实,益生菌可以刺激免疫细胞的免疫调节特性,维持免疫内环境平衡,调节胃肠道生态系统,是潜在的防治过敏性疾病的有效疗法。改变抗原提呈细胞的功能或调节Th1/Th2平衡是益生菌抗过敏的基本作用机制。目前益生菌防治过敏性疾病已经成为国内外研究的热点,未来有望利用益生菌实现过敏性疾病的个性化与精准化治疗。本文就益生菌防治过敏性疾病的最新进展以及该领域前沿作一综述,期望有助于我国益生菌治疗和预防过敏性疾病的普及和研究。     

The two faces of mast cells in food allergy and allergic asthma: The possible concept of Yin Yang

The purpose of this review is to discuss the role of mast cells in allergic inflammation. We have focused on inflammation associated with allergic asthma and food allergy. Mast cells are ‘first line of defense’ innate/adaptive immune cells and are widely distributed in tissues in surfaces exposed to the environment. Especially in allergic settings mast cells are extensively studied, as they can be activated to release a wide range of mediators by allergen-IgE specific triggers. In addition, in allergic inflammation mast cells can also be activated non-allergic triggers. Recent studies revealed that mast cells, besides the classical role of pro-inflammatory effector cell, have also emerged as modulators of allergic sensitization and down-regulators of allergic inflammation. Therefore, mast cells can be regarded as ‘Ying Yan’ modulators in allergic responses in intestinal tract and airways. This article is part of a Special Issue entitled: Mast Cells in Inflammation.     

Environmental factors and allergic airway diseases

A number of epidemiological studies show that in the last few decades, all over Europe, there has been a growing increase in allergic respiratory disease, which affects between 15 to 30% of the population. There is compelling evidence that this rise in allergic illnesses depends mainly on the type of the environmental pollution and on the typical lifestyle of western countries. Community-based studies comparing people living in former East and West Germany have proved a high prevalence of allergic respiratory disease in West German cities, with variances due to the differences in indoor and outdoor pollution. Ozone, nitrogen oxides, and respirable particulate matter (PM10) are the main components of photochemical smog, typical of western countries. They can lead to sensitization and the onset of allergic illnesses with direct and indirect mechanisms. The casual relationship between automobile traffic-generated pollution, in particular diesel exhaust particles which act as adjuvant on pollen sensitization, and the increase in allergic sensitization to pollens was proved by epidemiological observations, which were later confirmed by studies of animal laboratory exposure. Indoor environment is probably as important in increasing the prevalence of allergic disease. Different housing habits, energy-efficient buildings, and modern air-handling systems have reduced ventilation and produced substantial changes in indoor environment and an increased exposure to allergens (housedust mites, mould and pets dander in particular). Like outdoor pollution, tobacco smoke, formaldehyde, volatile organic compounds, fire burning products, and other chemicals can enhance allergic sensitization with direct and indirect mechanisms. Increased exposure to allergens in the early years of life can influence the immune regulation and the evolution towards a prevailing Th2 response. Recent epidemiological observations lead us to conclude that in the onset of allergic airway illnesses environmental factors can play a greater role than genetic predisposition. This revised version was published online in June 2006 with corrections to the Cover Date.     

Initial high-dose nasal allergen exposure prevents allergic sensitization to a neoantigen

Primary allergic sensitization--IgE formation after Ag exposure--is fundamental in the development of allergic respiratory disease. With the rising prevalence of asthma and allergic rhinitis, improved understanding of the determining factors for allergic sensitization is needed. Human epidemiologic studies suggest high-dose allergen exposure may paradoxically protect against sensitization. Prospective human studies of allergen dose effect on primary allergic sensitization are lacking. We prospectively examined the effect of respiratory Ag dose exposure on the rate of primary allergic sensitization to a neoantigen, keyhole limpet hemocyanin, using a unique model of human nasal allergic sensitization. Atopic human subjects were exposed to 0.1-, 10-, 1,000-, or 100,000-mug doses of intranasal keyhole limpet hemocyanin in conjunction with adjuvant intranasal diesel exhaust particles. Ag-specific IgE, IgG, and IgG4 were measured in nasal lavage samples at the conclusion of the sensitization protocol. Allergic sensitization rates for the 0.1-, 10-, 1,000-, and 100,000-mug dose groups were 0, 100, 57, and 11%, respectively. All subjects produced Ag-specific IgG with the highest levels observed in the high-dose group. These results provide direct evidence that primary allergic sensitization may be prevented by initial high levels of respiratory Ag exposure through induction of a modified, nonallergic immune response. This Ag dose effect was capable of overcoming the well-established allergic adjuvant effects of diesel exhaust particle exposure. Whether this immune response represents durable allergic tolerance is not yet known. Studies investigating the molecular mechanisms of this non-IgE response may be useful in developing therapy to prevent allergic sensitization.     

Replication of genome-wide association studies on asthma and allergic diseases in Korean adult population

Allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis are heterogeneous diseases characterized by multiple symptoms and phenotypes. Recent advancements in genetic study enabled us to identify disease associated genetic factors. Numerous genome-wide association studies (GWAS) have revealed multiple associated loci for allergic diseases. However, the majority of previous studies have been conducted in populations of European ancestry. Moreover, the associations of single nucleotide polymorphisms (SNPs) with allergic diseases have not been studied amongst the large-scale general Korean population. Herein, we performed the replication study to validate the previous variants, known to be associated with allergic diseases, in the Korean population. In this study, we categorized three allergic related phenotypes, one allergy and two asthma related phenotypes, based on self-reports of physician diagnosis and their symptoms from 8,842 samples. As a result, we found nominally significant associations of 6 SNPs with at least one allergic related phenotype in the Korean population.     

Air pollution and allergic airway diseases

In the last decades, many studies have shown an increase in the prevalence of allergic rhinitis and asthma mainly in urban communities, especially in industrialized countries. Airborne pollutants such as diesel exhaust particles, ozone, nitrogen dioxide and sulphur dioxide have been implicated in the initiation and exacerbation of allergic airway diseases. Epidemiologic studies have shown clear associations between air pollution and allergic diseases, in vivo and in vitro studies have provided biologic link and potential molecular mechanisms. Particulate and gaseous pollutants can act both on the upper and lower airways to initiate and exacerbate cellular inflammation through interaction with the innate immune system. As a consequence, increased non-specific airway hyper-responsiveness and airway resistance have been observed in man. Diesel exhaust particles can both induce and exacerbate in vivo allergic responses. They can also modify the immune system's handling of the allergen. The effects of gaseous pollutants on immune responses to allergens are not fully understood. We review the different mechanisms involved in the enhancement of allergic inflammation by urban air pollutants, including effects on cytokine and chemokine production, as well as activation of different immune cells. We discuss the hypothesis that pollutants' effects on the immune system involve hierarchical oxidative stress. Susceptibility genes to air pollution inducing allergic diseases are also discussed.     

Plasma kallikrein during experimentally induced allergic rhinitis: role in kinin formation and contribution to TAME-esterase activity in nasal secretions

We have shown recently that kinins are generated during experimentally induced allergic rhinitis in man, and have demonstrated that substrates for kinin-forming enzymes are provided during the allergic response by a transudation of kininogens from plasma into nasal secretions. In light of this increased vascular permeability during the allergic reaction, we have extended our studies on the mechanisms of kinin formation to examine the potential involvement of plasma kallikrein. Allergic individuals (n = 7) and nonallergic controls (n = 7) were challenged intranasally with an allergen, and nasal lavages, obtained before and after challenge, were assayed for immunoreactive human plasma kallikrein/prekallikrein (iHPK). Post-challenge iHPK values were significantly elevated (p less than 0.01) in the allergic group (353 +/- 394 ng/ml; x +/- SD) as compared to the nonallergics (19 +/- 22 ng/ml), and correlated with increases in kinins, histamine, and N-alpha-tosyl-L-arginine methyl esterase (TAME-esterase) activity and with the onset of clinical symptoms. Gel filtration studies revealed that plasma prekallikrein is activated during the allergic response and contributes to kinin formation prior to interaction with plasma protease inhibitors. We also show that the majority of the TAME-esterase activity detected in nasal secretions during the allergic response is due to activities consistent with a plasma kallikrein/alpha 2-macroglobulin complex and with mast cell tryptase.     

Active or Passive Exposure to Tobacco Smoking and Allergic Rhinitis, Allergic Dermatitis,and Food Allergy in Adults and Children: A Systematic Review and Meta-Analysis

BackgroundAllergic rhinitis, allergic dermatitis, and food allergy are extremely common diseases, especially among children, and are frequently associated to each other and to asthma. Smoking is a potential risk factor for these conditions, but so far, results from individual studies have been conflicting. The objective of this study was to examine the evidence for an association between active smoking (AS) or passive exposure to secondhand smoke and allergic conditions.ConclusionsWe observed very modest associations between smoking and some allergic diseases among adults. Among children and adolescents, both active and passive exposure to SHS were associated with a modest increased risk for allergic diseases, and passive smoking was associated with an increased risk for food allergy. Additional studies with detailed measurement of exposure and better case definition are needed to further explore the role of smoking in allergic diseases.Please see later in the article for the Editors'' Summary     

Allergic rhinitis: evidence for impact on asthma

Background

This paper reviews the current evidence indicating that comorbid allergic rhinitis may have clinically relevant effects on asthma.

Discussion

Allergic rhinitis is very common in patients with asthma, with a reported prevalence of up to 100% in those with allergic asthma. While the temporal relation of allergic rhinitis and asthma diagnoses can be variable, the diagnosis of allergic rhinitis often precedes that of asthma. Rhinitis is an independent risk factor for the subsequent development of asthma in both atopic and nonatopic individuals. Controlled studies have provided conflicting results regarding the benefits for asthma symptoms of treating comorbid allergic rhinitis with intranasal corticosteroids. Effects of other treatments for comorbid allergic rhinitis, including antihistamines, allergen immunotherapy, systemic anti-IgE therapy, and antileukotriene agents, have been examined in a limited number of studies; anti-IgE therapy and antileukotriene agents such as the leukotriene receptor antagonists have benefits for treating both allergic rhinitis and asthma. Results of observational studies indicate that treating comorbid allergic rhinitis results in a lowered risk of asthma-related hospitalizations and emergency visits. Results of several retrospective database studies in the United States and in Europe indicate that, for patients with asthma, the presence of comorbid allergic rhinitis is associated with higher total annual medical costs, greater prescribing frequency of asthma-related medications, as well as increased likelihood of asthma-related hospital admissions and emergency visits. There is therefore evidence suggesting that comorbid allergic rhinitis is a marker for more difficult to control asthma and worsened asthma outcomes.

Conclusion

These findings highlight the potential for improving asthma outcomes by following a combined therapeutic approach to comorbid allergic rhinitis and asthma rather than targeting each condition separately.

     

Current directions of studies for development of methods for specific diagnostics of allergic diseases in vitro

Results of studies as well as perspectives for development and use of modern in vitro methods of allergic diseases diagnostics are presented. High prevalence of allergic diseases dictates the need of high-quality etiologic diagnosis for conducting relevant etiopathogenetic treatment - allergen-specific immunotherapy and prophylactic measures. Interest to in vitro diagnostic methods due to their high specificity and commonality is rising. They are directed to identification of various elements of "material substrate" of allergic reaction - specific antibodies, cell elements, cytokines as well as genes, which encode them. Intensively developing methods based on immunoenzyme, immunofluorescent, and immunochemiluminescent reactions are widely used now. Methods based on the use of various monoclonal antibodies for identification of lymphocytic markers, cytokines, antigen-presenting cells by laser flowcytometry are also very promising. ELISPOT technology is also intensively used for diagnostics of allergic diseases. From immunogenetic methods great potential belongs to molecular biologic methods of assessment of genome specificity characterizing sensitization to given antigen.     

Cyclooxygenase inhibition during allergic sensitization increases STAT6-independent primary and memory Th2 responses

Immune sensitization and memory generation are required for the development of allergic inflammation. Our previous studies demonstrate that the cyclooxygenase (COX) metabolic pathway is actively involved in allergic responses and COX inhibition increases allergic airway inflammation in a STAT6-independent fashion. To test the hypothesis that COX inhibition augments allergic inflammation by enhancing immune sensitization and memory, we sensitized STAT6 knockout mice with an i.p. injection of OVA with aluminum hydroxide as an adjuvant and treated the mice with the COX inhibitor indomethacin or vehicle for analyses of the primary and memory immune responses. We found that COX inhibition during immune sensitization, but not the allergic challenge phase, was necessary and sufficient to increase allergic inflammation. COX inhibition during sensitization increased the numbers of mature dendritic cells and activated CD4 T cells in the spleen and augmented OVA-specific IL-5 and IL-13 responses of the splenic CD4 T cells at day 5 after sensitization. COX inhibition during sensitization also augmented allergic Th2 response to OVA challenge 90 days after the sensitization. Therefore, COX inhibition during allergic sensitization augments allergic responses by enhancing Th2 cell activation and memory generation and the proallergic effect is STAT6-independent. These findings provide a mechanistic explanation for the increased allergic inflammation previously shown in the mice treated with COX inhibitors and in COX-deficient mice and suggest that use of COX-inhibiting drugs during initial allergen exposure may increase the risk of developing allergic responses.