Lactoferrin Ameliorates Ovalbumin-Induced Asthma in Mice through Reducing Dendritic-Cell-Derived Th2 Cell Responses

Asthma is a chronic respiratory disease with symptoms such as expiratory airflow narrowing and airway hyperresponsiveness (AHR). Millions of people suffer from asthma and are at risk of life-threatening conditions. Lactoferrin (LF) is a glycoprotein with multiple physiological functions, including antioxidant, anti-inflammatory, antimicrobial, and antitumoral activities. LF has been shown to function in immunoregulatory activities in ovalbumin (OVA)-induced delayed type hypersensitivity (DTH) in mice. Hence, the purpose of this study was to investigate the roles of LF in AHR and the functions of dendritic cells (DCs) and Th2-related responses in asthma. Twenty 8-week-old male BALB/c mice were divided into normal control (NC), ovalbumin (OVA)-sensitized, and OVA-sensitized with low dose of LF (100 mg/kg) or high dose of LF (300 mg/kg) treatment groups. The mice were challenged by intranasal instillation with 5% OVA on the 21st to 27th day after the start of the sensitization period. The AHR, cytokines in bronchoalveolar lavage fluid, and pulmonary histology of each mouse were measured. Serum OVA-specific IgE and IgG1 and OVA-specific splenocyte responses were further detected. The results showed that LF exhibited protective effects in ameliorating AHR, as well as lung inflammation and damage, in reducing the expression of Th2 cytokines and the secretion of allergen-specific antibodies, in influencing the functions of DCs, and in decreasing the level of Th2 immune responses in a BALB/c mouse model of OVA-induced allergic asthma. Importantly, we demonstrated that LF has practical application in reducing DC-induced Th2 cell responses in asthma. In conclusion, LF exhibits anti-inflammation and immunoregulation activities in OVA-induced allergic asthma. These results suggest that LF may act as a supplement to prevent asthma-induced lung injury and provide an additional agent for reducing asthma severity.     

IL-33 and IL-37: A Possible Axis in Skin and Allergic Diseases

Interleukin (IL)-37 and IL-33 are among the latest cytokines identified, playing a role in several inflammatory conditions, spanning from systemic conditions to tumors to localized diseases. As newly discovered interleukins, their role is still scarcely understood, but their potential role as therapeutic targets or disease activity markers suggests the need to reorganize the current data for a better interpretation. The aim of this review is to collect and organize data produced by several studies to create a complete picture. The research was conducted on the PubMed database, and the resulting articles were sorted by title, abstract, English language, and content. Several studies have been assessed, mostly related to atopic dermatitis and immunologic pathways. Collective data demonstrates a pro-inflammatory role of IL-33 and an anti-inflammatory one for IL-37, possibly related to each other in an IL-33/IL-37 axis. Although further studies are needed to assess the safety and plausibility of targeting these two interleukins for patients affected by skin conditions, the early results indicate that both IL-33 and IL-37 represent markers of disease activity.     

银杏叶提取物对哮喘儿童血小板活化因子水平的影响

采用银杏叶提取物和激素分别治疗25例儿童支气管哮喘。检测患儿治疗前后血浆血小板活化因子(PAF)水平,观察哮喘临床症状改善情况并与激素治疗组儿童血浆PAF水平比较。结果表明:银杏叶提取物治疗后,支气管哮喘患儿血浆PAF水平与激素治疗组患儿PAF水平无显著性差异(t=0.997,p>0.05),哮喘改善时间接近,银杏叶提取物可能是一种新型的预防和治疗支气管哮喘的药物。     

Cobalt-related asthma: clinical and immunological aspects

Several clinical and experimental findings point to cobalt as the only sensitizer and causal agent of hard metal asthma. The clinical features have been clearly defined by bronchial provocation tests, with a prevalence of late phase responses. Epidemiology is still insufficient to configure prevalence and incidence rates for cobalt asthma. IgE and IgG antibodies with cobalt specificity have been demonstrated, but T-lymphocytes and eosinophyls involvement seem to be important in the mechanism of an allergic inflammation in the airways. Such an immunological pathogenesis links cobalt asthma with other manifestation of hard metal disease.     

Proposing a decision support system for automated mobile asthma monitoring in remote areas*

ABSTRACT

Advances in mobile computing have paved the way for the development of several health applications using Smartphone as a platform for data acquisition, analysis and presentation. Such areas where m-health systems have been extensively deployed include monitoring of long-term health conditions such as cardio-vascular diseases and pulmonary disorders, as well as detection of changes from baseline measurements of such conditions. Asthma is one of the respiratory conditions with growing concern across the globe due to the economic, social and emotional burden associated with the ailment. The management and control of asthma can be improved by consistent monitoring of the condition in real-time since attack could occur anytime and anywhere. This paper proposes the use of smartphone equipped with built-in sensors, to capture and analyze early symptoms of asthma triggered by exercise. The system design is based on decision support system (DSS) techniques for measuring and analyzing the level and type of patient’s physical activity as well as weather conditions that predispose asthma attack. Preliminary results show that smartphones can be used to monitor and detect asthma symptoms without other networked devices. This would enhance the usability of the health system while ensuring user’s data privacy, and reducing the overall cost of system deployment. Further, the proposed system can serve as a handy tool for a quick medical response for asthmatics in low-income countries where there is limited access to specialized medical devices and shortages of health professionals. Development of such monitoring systems signals a positive response to lessen the global burden of asthma.     

罗红霉素与布地奈德干粉吸入剂联用治疗哮喘的临床研究

目的:通过与单纯吸入布地奈德干粉吸入剂(普米克都保)组比较, 观察口服罗红霉素联用布地奈德干粉吸入剂治疗哮喘的疗效及对血清可溶性IL-2 受体(sIL-2R)、IL-8 和血嗜酸性粒细胞(EOS)计数水平的影响。方法:选择门诊轻、中度急性发作哮喘患者45 例, 随机分组。治疗组口服罗红霉素联合吸入布地奈德干粉吸入剂, 对照组吸入布地奈德干粉吸入剂, 疗程4 周。治疗前、治疗4 周后检测肺功能、血sIL-2R 、IL-8 和EOS 计数水平, 并按临床症状记分。结果:40 例完成了试验, 治疗4 周后临床症状记分、肺功能一秒钟用力呼气量(FEV₁)、FEV₁ 占预计值百分比(FEV₁/pred %)、最大呼气流量(PEF)和PEF 占预计值百分比(PEF/pred %)改善, 血sIL-2R 、IL-8 和EOS 计数水平较治疗前降低, 且治疗组较对照组改善更为明显, 两组副作用相似。结论:罗红霉素具有抗炎和免疫调节作用, 罗红霉素与布地奈德干粉吸入剂联用可以提高疗效。     

黄芪注射液对哮喘大鼠p38蛋白激酶和白细胞介素-5表达的影响

目的:探讨黄芪注射液对哮喘大鼠p38蛋白激酶(p38 MAPK)和白细胞介素-5(IL-5)表达的影响。方法:应用鸡卵清蛋白(OVA)腹腔注射致敏和反复超声雾化吸入复制大鼠哮喘模型。40只大鼠随机分成5组:正常对照组, 哮喘模型组和黄芪注射液低、中、高剂量组(2.5、5.0、10.0 mL/kg)。分别采用酶联免疫吸附法(ELISA)、原位分子杂交方法和蛋白质印迹检测支气管肺泡灌洗液(BALF)IL-5含量、肺组织IL-5 mRNA和磷酸化p38 MAPK 表达的变化, 并观察BALF 中炎症细胞计数、分类以及肺组织病理学变化。结果:哮喘模型组大鼠BALF 中炎症细胞计数、IL-5含量和肺组织中IL-5 mRNA及磷酸化p38 MAPK 表达均较正常对照组显著增加(P<0.01);黄芪干预组的上述改变较哮喘模型组显著降低(P<0.01), 肺组织病理学损伤程度明显减轻, 黄芪注射液低、中、高剂量组之间差异无统计学意义。肺组织磷酸化p38 MAPK 表达水平与BALF中嗜酸性粒细胞(EOS)计数和IL-5、IL-5 mRNA含量之间分别呈显著正相关(r=0.62、0.69、0.74, P<0.01)。结论:p38 MAPK 可能参与了支气管哮喘的发病过程。黄芪对哮喘的治疗作用可能部分与抑制p38 MAPK 的磷酸化活化、降低炎症介质释放、减轻炎症细胞浸润有关。     

砒石对哮喘小鼠白三烯B4 及5-脂氧合酶基因表达的影响

目的: 探讨白三烯B4 (LTB4) 水平、5-脂氧合酶(5-LO) 基因表达在小鼠哮喘发病中的作用以及砒石(arsenolite, As) 对哮喘的治疗作用与LTB4 水平及5-LO 基因表达的关系。方法: 建立小鼠卵蛋白哮喘模型, 灌胃给予砒石等药, 用ELISA 的方法检测支气管肺泡灌洗液(BALF) LTB4 含量;用RT-PCR 的方法检测肺组织中5-LO mRNA 表达的变化。结果: 哮喘小鼠BALF 中LTB4 水平、肺组织5-LO 基因表达水平较正常对照组显著升高。4 种剂量的砒石均可抑制哮喘小鼠BALF 中LTB4 的水平, 均能降低哮喘小鼠5-LO mRNA 表达的量。其中砒石5.00 mg·kg^-1 剂量的效果优于砒石0.625 mg·kg^-1剂量的效果。结论: LTB4 在气道中的高水平, 5-LO 基因表达的上调在OVA 致敏小鼠的哮喘发病中起重要作用。砒石可显著降低哮喘小鼠BALF 中LTB4 水平, 抑制哮喘小鼠肺组织中5-LO 基因的表达, 从而表现出抗哮喘的活性。     

抗哮喘免疫乳研究初报

哺乳动物的乳汁是机体免疫协调作用分泌产物之一，新生动物可以通过乳中的抗体获得被动免疫抵抗病原微生物的感染。因此，我们也可以应用乳中的特异抗体预防和治疗某些疾病。本课题组用气管炎疫苗免疫妊娠后期奶牛抗哮喘的免疫乳，并用ELISA法测定了特定抗体的含量。     

Effects of paternal and maternal depressive symptoms on child internalizing symptoms and asthma disease activity: Mediation by interparental negativity and parenting.

This study tested a hypothesized model of the relationships among parental depressive symptoms, family process (interparental negativity and negative parenting behavior), child internalizing symptoms, and asthma disease activity. A total of 106 children with asthma, aged 7 to 17, participated with their fathers and mothers. Parental depressive symptoms were assessed by self-report. Interparental and parenting behaviors were observed and rated during family discussion tasks. Child internalizing symptoms were assessed by self-report and by clinician interview and rating. Asthma disease activity was assessed according to National Heart, Lung and Blood Institute guidelines. Results of structural equation modeling generally supported interparental negativity and negative parenting behavior as mediators linking parental depressive symptoms and child emotional and physical dysfunction. However, paternal and maternal depressive symptoms play their role through different pathways of negative family process. (PsycINFO Database Record (c) 2011 APA, all rights reserved)