2016, Vol. 30
变应性疾病(allergic diseases,AR)在各年龄段及不同种族的人群中均有发病，临床常见的变应性疾病主要包括哮喘、变应性鼻炎和湿疹等[1]。近年来，变应性疾病的发病率逐年上升，全球范围内约有3亿人口患有哮喘[2]，约6.8亿人罹患湿疹，约20亿人患有变应性鼻炎[3-4]。变应性疾病的临床症状严重影响患者的生活质量，甚至危及患者生命(如重症哮喘)。世界变态反应组织(world allergy organization，WAO)的相关报告显示，现代生活方式的人们约90%的时间生活和工作在室内，而室内环境污染程度比室外高2～5倍，因此室内空气污染物成为变应性疾病的高危因素[5]。此外，西方化饮食结构也可促进变应性疾病的发生[6-11]。现综述几种主要室内污染物及饮食结构对变应性疾病的影响，并阐述其可能的发病机制。
1 室内空气污染物与变应性疾病 1.1 环境烟草烟雾(environmentaltobacco smoke，ETS) ETS是主要的室内空气污染物[12]，常被称为“二手烟”(secondhand smoking，SHS)，由烟草制品(香烟、雪茄等)燃烧产生。据世界卫生组织估计，全球约有1/3的成人和40%儿童长期接触ETS[13]。流行病学数据显示，环境烟草烟雾与变应性疾病的发病显著相关。Feleszko等[14]进行的系统性回顾研究指出，ETS暴露是变应性疾病发病的重要危险因素，可增加罹患变应性疾病的风 险。一项对3 316名新生儿进行的长达16年的跟踪调查发现，婴儿期ETS暴露时间与湿疹的发病率呈正相关(OR： 1.62，95%CI: 1.20～2.18)[15]。美国马里兰州的Shargorodsky等[16]检测当地4 339名成人(20~85岁)体内血清可替尼浓度并进行统计分析后发现，血清可替尼浓度与变应性鼻炎的发病率呈正相关(OR: 1.42，95%CI: 1.00～2.00)。Andrews等[17]对623名哮喘儿童(41%有SHS暴露史)的住院时间进行统计，发现与非暴露组相比，SHS暴露组的平均住院时间延长4.2 h。
但是，Abramson等[18]进行的调查问卷结果显示，SHS暴露与变应性鼻炎无明显相关性。Shargorodsky等[19]对全国健康和营养调查(The National Health and Nutrition Examination Survey，NHANES)资料数据进行横断面分析后，认为ETS暴露降低了机体过敏反应的发生率。以上差异可能与数据处理方式、地域、性别及个体差异有关。
1.2 挥发性有机化合物(volatile organic compounds, VOCs)挥发性有机化合物是室内环境污染物之一，主要由甲醛、C8-芳香族化合物(二甲苯和乙基苯等)以及甲苯等数十种有机化学物质组成，广泛存在于家居油漆、木材、纤维织物、清洁剂、空气清新剂、化妆品、家具、地板和墙面装饰物中，并随室内温度的升高而释放。据美国国家环境保护局报道，室内家居的VOCs含量比室外高出5～10倍[20]。诸多临床研究表明VOCs与变应性疾病相关，德国萨克森州Herberth等[21]对6 565名6周岁儿童进行问卷调查并随机采集324名儿童血样进行分析后发现，VOCs可使外周血中IL-8和MCP-1水平升高，从而引发气道炎症反应。一项针对400名儿童(198名患有哮喘或其他过敏疾病，202名健康儿童作为对照)进行的对照研究发现[22]，长期VOCs暴露可引发机体发生氧化应激反应，加重哮喘、变应性鼻炎和湿疹等变应性疾病的症状。日本学者对988名孕妇进行数据采集及统计学分析发现，甲醛(浓度≥47 ppb)可以增加变应性鼻炎的罹患率(OR: 2.25，95%CI: 1.01～5.01)[23]。法国室内空气质量观测站统计了490个主要居民区20种VOC的室内水平，并对1 012名长期居住居民(≥15年)进行标准化问卷调查，发现VOCs得分与哮喘(OR 1.4)和变应性鼻炎(OR 1.22)的发病呈正相关[24]。
但是，Venn等[25]收集英国诺丁汉地区416名儿童(含193名哮喘儿童)所处家居环境资料并进行统计学分析，发现仅甲醛浓度与夜间出现喘息症状的次数相关，而其他种类VOCs与喘息性疾病的发病无明显相关性。曼彻斯特一项针对200名儿童的病例-对照研究发现，VOCs与哮喘等变应性疾病的发病无相关性[26]。另一项来自曼彻斯特的问卷调查研究同样显示，VOCs对儿童哮喘的发病无显著的统计学意义[27]。
1.3 气传变应原(aeroallergens)上世纪60年代有研究开始关注气传变应原与变应性疾病的关系，目前已有相关检测应用于临床试验。尘螨、花粉、霉菌和宠物毛发是主要的气传变应原[28-29]。在工业化国家，对气传变应原敏感的人群数量大幅上升[30-31]。
Mbatchou Ngahane等[32]以喀麦隆杜阿拉大学医学及药学院的600名学生(305女性)作为研究对象进行问卷调查，结果显示尘螨等气传变应原与哮喘和变应性鼻炎的发病均具有相关性。墨西哥新昂莱州Yong-Rodríguez等[33]进行的回顾性研究显示，具有高蛋白酶活性的气传变应原与湿疹的发病有关。Pefura-Yone等[34]对523名受试对象(其中151名哮喘患者)进行的病例对照研究发现，尘螨过敏与哮喘的发病显著相关。瑞典Patelis等[35]的最新研究发现，哮喘的发病与气传变应原的颗粒大小有关，其颗粒直径越小诱发哮喘的风险越高。
2 饮食结构与变应性疾病西方饮食结构以肉类和高热量食物为主，其中含有大量多价不饱和脂肪酸和胆固醇，而缺乏植物纤维素及维生素C、E等微量元素。N-6 PUFA 亚油酸(linoleicacid，LA)作为多价不饱和脂肪酸是花生四烯酸的前体物，富含于动物肌肉及植物油中，是前列腺素(prostaglandin，PG)E2和白三烯(leukotriene，LT)B4等炎性介质的合成原料，大量摄取可能促发变应性炎症[36]。Julia等[37]指出，均衡饮食结构可诱导机体产生“口服耐受”，维持机体的免疫稳态、防止变应性疾病的发生；而高卡路里、低纤维素和微量元素摄入则引发机体次级代谢产物的改变，从而诱发变应性疾病。
Ellwood等[6]对青少年和儿童进行问卷调查并用Logistic回归进行统计学分析，发现西式快餐摄入(≥3次/周)与哮喘、鼻炎以及湿疹的发病呈正相关。Wood等[7]针对哮喘患者进行的病例对照研究表明，大量脂肪摄入可以引发哮喘患者的支气管炎症并弱化支气管扩张剂的作用。Alfonso等[8]发现，以高热量食物为主的西方快餐摄入量与哮喘喘息症状的发生次数呈正相关(OR: 1.76，95%CI: 1.32～2.35，P=0.001)。
“地中海型”饮食结构以蔬菜、淀粉、水果、橄榄油及鱼类为主。近年来，我国学者认为蔬菜、水果等食物中的抗氧化剂如黄酮类(navonoid)中的花色甙(anthocyanins)和根皮素(phloridzin),维生素C、E、A和硒等可通过调节免疫和气道氧化损伤减少呼吸道变应性疾病的发病和减轻病情[38]。N-3 PUFA α-亚麻酸(α-linolenicacid，LNA)在大豆制品、鱼类及贝类中含量较高，其代谢产物EPA和DHA富含于鱼油中，可抑制PGE2和LTB4的合成[36]。
Alfonso等[8]对哥伦比亚3209名参与“儿童过敏及哮喘国际性研究(ISAAC)”的儿童数据进行统计学分析，发现新鲜水果摄入与湿疹的发病呈负相关(OR: 0.64，95%CI: 0.49～0.83，P=0.004)。Chatzi等[9-10]研究发现，“地中海型”饮食可降低哮喘和变应性鼻炎的发病率。Wood等[11]针对137名哮喘患者进行随机分组对照试验，发现适量摄入富含胡萝卜素的水果和蔬菜可改善哮喘的临床症状。
但是，土耳其的Tamay等[39-40]对参与ISAAC的9 991名青少年及11 483名儿童进行问卷调查，发现“地中海”型饮食结构对土耳其当地儿童及青少年变应性鼻炎的发病率并无影响。二者的关系尚待进一步探讨。
3 可能的发病机制 3.1 AhR信号通路介导的细胞调控AhR(Aryl hydrocarbon Receptor)是来自PAS家族的配体激活转录因子，可维持细胞稳态[41-42]，也可作为环境污染物(如联苯、多氯联苯等)的受体。Hao等[43]认为，环境毒素(如二噁英等化合物)可激活AhR，诱导Th1/Th2失衡，抑制Treg细胞，从而引发免疫性疾病。Zhou等[44]检测哮喘患者肺成纤维细胞的AhR蛋白表达水平，发现与对照组相比，哮喘患者的AhR蛋白表达明显上调，AhR激活后体内cyp1a1及cyp1b1蛋白表达上调，进而调控机体免疫平衡。Wei等[45]发现，变应性鼻炎患者体内AhR表达上调，进而影响Th17细胞功能，从而导致变应性鼻炎发生。Veldhoen等[46]及Quintana等[47]2008年发表于《Nature》的文章指出，AhR可影响NF-κB、MAPK、STAT1和STAT5等信号因子以及相关免疫细胞如Th17、Treg、肥大细胞和树突状细胞等，进一步诱发变应性疾病。由此可见，AhR信号通路是连接环境污染物与变应性疾病的桥梁，外界影响因素可直接或间接作用于AhR而引起变应性疾病。
3.2 氧化应激反应Sim等[48]针对90名儿童的病例-对照研究指出，变应性鼻炎患者的氧化应激指数(TOS/TAS)普遍增高，并存在系统性氧化应激反应。Ling等[49]发现，环境中的过敏原及其他物质可诱发人体嗜碱性粒细胞介导的氧化应激反应，从而引发哮喘及其他变应性疾病。Jiang等[50]认为，环境污染物暴露促使体内产生过量活性氧(reactive oxygen species，ROS)，从而破坏DNA、蛋白质及脂质的功能，引发哮喘。另有研究指出[51]，暴露于室内污染物或摄入高脂类食物可直接刺激机体产生ROS及其二级产物，或通过“芬顿反应”(过氧化氢与二价铁离子的混合溶液,具有强氧化性，可将有机化合物如羧酸、醇及酯类氧化为无机态)间接产生ROS。ROS通过影响细胞转录信号通路及转录因子(如MAPK激酶、磷酸肌醇-3激酶、NF-κB和AP-1)，促使炎症介质的转录及表达[52-53]，从而导致呼吸道黏膜炎症反应等病理改变。
3.3 表观遗传学改变斯坦福大学的Kohli等[54]研究证实，SHS暴露可引起DNA高度甲基化以及IFN-γ和Foxp3表达下调。Adenuga等[55]认为，SHS暴露使丝氨酸和苏氨酸磷酸化，下调Ⅱ型组蛋白去乙酰酶(histone deacetylase 2，HDAC2)表达，诱导机体产生激素抵抗和异常炎症反应，加重变应性疾病的临床症状并减弱治疗效果。相关动物实验表明，暴露于邻苯二甲酸二乙酯后，Balb/c小鼠体内CD4+ T细胞的IL-4及IFN-γ启动子甲基化水平增高，进而影响IgE水平[56]。Sofer等[57]发现，硫酸盐类物质暴露与哮喘相关信号通路甲基化显著相关(P=0.02)。Yang等[58]进行的对照试验发现，哮喘患者体内RUN X3、IL-4和IL-13基因的特定位点高度甲基化，可能与哮喘发病相关。
3.4 Th1与Th2细胞失衡早期研究发现，VOCs(甲醛、全氟化碳及增塑剂等)可活化Th2细胞并抑制Th1细胞，从而诱发或加重变应性疾病。相关研究表明，ETS暴露可减少IFN-γ生成并抑制NK细胞活性，从而降低Th1应答；同时增加IL-4、IL-5、IL-13和其他促炎因子的分泌，从而增强Th2细胞主导的免疫应答[59]。相关动物实验证实，暴露于壬基酚(Nonylphenol，NP)的小鼠脾脏DCs明显向Th2偏移，IL-6和TNF-α水平迅速增加。且NP暴露时骨髓来源的DCs可影响抗原特异性T细胞，显著减少IFN-γ分泌[60]，进而引发以Th2细胞为主导的变应性疾病。
3.5 肠道菌群作用研究表明，以植物油、淀粉及粗纤维为主的“地中海饮食”可升高肠道内益生菌含量。Lee等[61]发现，亚麻籽油摄入(≥8周)可使肠道内厚壁菌门数量升高，拟杆菌门数量降低。美国德克萨斯Lyte等[62]研究证实，摄入HA7型抗性淀粉可使小鼠肠道内双歧杆菌含量升高。澳大利亚昆士兰Williams等[63]研究发现，经AX型小麦饲养4周后，猪盲肠内柔嫩梭菌含量大幅上升。
目前研究采用的益生菌主要包括L.johnsonii、L.casei、L.rhamnosus、嗜酸性乳酸杆菌(L.acidophilus)、副干酪乳酸杆菌(L.paracasei)、保加利亚乳酸杆菌(L.bulgaricus)、长双歧杆菌(B.longum)、青春双歧杆菌(B.adolescentis)、嗜热链球菌(S.thermophilus)和粪肠球菌(E.faecalis)等[1]。
Shandilya等[64]发现，使用益生菌制剂后，小鼠体内Th1相关细胞因子表达上调，而Th2相关细胞因子表达下调，血清中IgE水平降低。张清照等[65]研究证实，益生菌提取物酶裂解的肠球菌faecalis FK-23菌株(lysed Enterococcus faecalis FK-23，LFK)对细胞因子IL-12具有调节作用。朱鲁平等[66]通过动物实验证实，益生菌可使小鼠血清和脾细胞培养液中的IFN-γ水平升高，IL-4水平降低，并下调血清OVA特异性IgE水平，从而改善变应性鼻炎症状。由此可见，适当增加肠道内益生菌含量可以防治变应性疾病,饮食结构可通过影响肠道内益生菌含量影响变应性疾病的发病。Takeda等[67]研究发现酪乳酸杆菌可促使人体内NK细胞的数目增多，在体内及体外水平均可增强NK细胞的活性。 Kwon等[68]研究发现，益生菌菌体与DC的结合后，可诱导不同类型DC的产生并促使其功能成熟。同时，益生菌可表达与肠道共生菌相同的PAMP，并可与表达在肠道淋巴组织上皮细胞和免疫辅助细胞(如DC和巨噬细胞)上的TLR相互结合[1]。由此可见，益生菌对免疫的调节作用包括：① 调节特异性体液免疫反应；② 识别Toll样受体；③ 调节NK细胞功能；④ 促进DC细胞分化和成熟。
综上，室内空气污染及饮食结构与变应性疾病的发病密切相关，相关研究从流行病学、表观遗传学等层面揭示了室内空气污染对变应性疾病的影响，以肉类、脂类摄入为主的西方化饮食已成为变应性疾病的危险因素。因此，注重和改善室内空气质量，适量补充维生素和蔬菜水果类食物，避免脂肪和高热量食物的过度摄入，对于变应性疾病的预防和治疗具有指导意义。
| [1] |
张清照, 朱鲁平, 程雷. 益生菌对变应性疾病的防治作用[J].
中华耳鼻咽喉头颈外科杂志,2013, 48 (7) : 604-608.
( 0)
|
| [2] |
Global Initiative for Asthma. Global strategy for asthma management and prevention[R]. GINA, 2012
(0)
|
| [3] |
World Allergy Organization White Book on Allergy 2011-2012[R].WAO, 2011
(0)
|
| [4] |
World Health Organization. Global surveillance, prevention and control of chronic respiratory diseases: a comprehensive approach[R]. Bousquet J, Khaltaev N. 2007.
(0)
|
| [5] |
Pawankar R, Canonica G W, Holgate S T, et al. WAO White book on allergy[R]. Milwaukee (WI): World Allergy Organization, 2011.
(0)
|
| [6] |
Ellwood P, Asher M I, García-Marcos L, et al. ISAAC Phase Ⅲ Study Group. Do fast foods cause asthma,rhinoconjunctivitis and eczema? Global findings from the International Study of Asthma and Allergies in Childhood (ISAAC)phase three[J].
Thorax,2013, 68 (4) : 351-360.
(0)
|
| [7] |
Wood L G, Garg M L, Gibson P G. A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma[J].
Allergy Clin Immunol,2011, 127 (5) : 1133-1140.
(0)
|
| [8] |
Cepeda A M, Del GiaccoS R, Villalba S, et al. A traditional diet is associated with a reduced risk of eczema and wheeze in colombian children[J].
Nutrients,2015, 7 (7) : 5098-5110.
(0)
|
| [9] |
Chatzi L, Kogevinas M. Prenatal and childhood Mediterranean diet and the development of asthma and allergies in children[J].
Public Health Nutr,2009, 12 (9A) : 1629-1634.
(0)
|
| [10] |
Chatzi L, Apostolaki G, Bibakis I, et al. Protective effect of fruits,vegetables and the Mediterranean diet on asthma and allergies among children in Crete[J].
Thorax,2007, 62 (8) : 677-683.
(0)
|
| [11] |
Wood L G, Garg M L, Smart J M, et al. Manipulating antioxidant intake in asthma: a randomized controlled trial[J].
Am J Clin Nutr,2012, 96 (3) : 534-543.
(0)
|
| [12] |
Wallace L A, Mitchell H, O'Connor G T, et al. Particle concentrations in inner-city homes of children with asthma: the effect of smoking,cooking,and outdoor pollution[J].
Environ Health Perspect,2003 .
(0)
|
| [13] |
World Health Organization. Second-hand smoke: assessing the burden of disease at national and local levels. Geneva: WHO Environmental Burden of Disease Series, No. 18[R]. Geneva: World Health Organization, 2008.
(0)
|
| [14] |
Feleszko W, Ruszczyński M, Jaworska J, et al. Environmental tobacco smoke exposure and risk of allergic sensitisation in children: a systematic review and meta-analysis[J].
Arch Dis Child,2014, 99 (11) : 985-992.
(0)
|
| [15] |
Thacher J D, Gruzieva O, Pershagen G, et al. Parental smoking and development of allergic sensitization from birth to adolescence[J].
Allergy,2015 .
doi: 10.1111/all.12792 (0)
|
| [16] |
Shargorodsky J, Garcia-Esquinas E, Galán I, et al. Allergic Sensitization,Rhinitis and Tobacco Smoke Exposure in US Adults[J].
PLoS One,2015, 10 (7) : e131957.
(0)
|
| [17] |
Andrews A L, Shirley N, Ojukwu E, et al. Is secondhand smoke exposure associated with increased exacerbation severity among children hospitalized forasthma?[J].
Hosp Pediatr,2015, 5 (5) : 249-255.
(0)
|
| [18] |
Abramson M J, Schindler C, Schikowski T, et al. Rhinitis in Swiss adults is associated with asthma and early life factors,but not second hand tobacco smoke or obesity[J].
Allergol Int,2015 .
doi: 10.1016/j.alit.2015.11.004. (0)
|
| [19] |
Shargorodsky J, Garcia-Esquinas E, Navas-Acien A, et al. Allergic sensitization, rhinitis, and tobacco smoke exposure in U.S. children and adolescents[J]. Int Forum Allergy Rhinol, 2015, 5(6):471-476.
(0)
|
| [20] |
U.S. Environmental Protection Agency. The Inside Story: A Guide to Air Quality[R]. Office of Radiation and Indoor Air (6609J): Washington, DC, USA, 2009.
(0)
|
| [21] |
Herberth G, Gubelt R, Rder S, et al. LISAplus study group. Increase of inflammatory markers after indoor renovation activities: the LISA birth cohort study[J]. Pediatr Allergy Immunol, 2009, 20(6):563-570.
(0)
|
| [22] |
Choi H, Schmidbauer N, Sundell J, et al. Common household chemicals and the allergy risks in pre-school age children[J].
PLoS One,2010, 5 (10) : e13423.
(0)
|
| [23] |
Matsunaga I, Miyake Y, Yoshida T, et al. Osaka Maternal and Child Health Study Group. Ambient formaldehyde levels and allergic disorders among Japanese pregnant women: baseline data from the Osaka maternal and child health study[J].
Ann Epidemiol,2008, 18 (1) : 78-84.
(0)
|
| [24] |
Billionnet C, Gay E, Kirchner S, et al. Quantitative assessments of indoor air pollution and respiratory health in a population-based sample of French dwellings[J].
Environ Res,2011, 111 (3) : 425-434.
(0)
|
| [25] |
Venn A J, Cooper M, Antoniak M, et al. Effects of volatile organic compounds,damp,and other environmental exposures in the home on wheezing illness in children[J].
Thorax,2003, 58 (11) : 955-960.
(0)
|
| [26] |
Gee I L, Watson A F R, Tavernier G, et al. Indoor air quality,environmental tobacco smoke and asthma: a case control study of asthma in a community population[J].
Indoor Built Environ,2005, 14 (2) : 215-219.
(0)
|
| [27] |
Tavernier G, Fletcher G, Gee I, et al. IPEADAM study: indoor endotoxin exposure,family status,and some housing characteristics in English children[J].
Allergy Clin Immunol,2006, 117 (3) : 656-662.
(0)
|
| [28] |
Singh A B, Kumar P. Aeroallergens in clinical practice of allergy in India. An overview[J].
Ann Agric Environ Med,2003, 10 (2) : 131-136.
(0)
|
| [29] |
Fereidouni M, Hossini R F, Azad F J, et al. Skin prick test reactivity to common aeroallergens among allergic rhinitis patients in Iran[J].
Allergol Immunopathol (Madr),2009, 37 (2) : 73-79.
(0)
|
| [30] |
Salo P M, Arbes S J Jr, Jaramillo R, et al. Prevalence of allergic sensitization in the United States: results from the National Health and Nutrition Examination Survey (NHANES) 2005-2006[J].
Allergy Clin Immunol,2014, 134 (2) : 350-359.
(0)
|
| [31] |
Dottorini M L, Bruni B, Peccini F, et al. Skin prick-test reactivity to aeroallergens and allergic symptoms in an urban population of central Italy: a longitudinal study[J].
Clin Exp Allergy,2007, 37 (2) : 188-196.
(0)
|
| [32] |
Mbatchou Ngahane B H, Noah D, Nganda Motto M, et al. Sensitization to common aeroallergens in a population of young adults in a sub-Saharan Africa setting: a cross-sectional study[J].
Allergy Asthma Clin Immunol,2016, 12 (1) : 1.
(0)
|
| [33] |
Yong-Rodríguez A, Macías-Weinmann A, Palma-Gómez S, et al. Profile of sensitization to allergens in children with atopic dermatitis assisting to Allergology Service of University Hospital,Nuevo Leon,Mexico[J].
Rev Alerg Mex,2015, 62 (2) : 98-106.
(0)
|
| [34] |
Pefura-Yone E W, Mbele-Onana C L, Balkissou A D, et al. for Groupe Enquête en Santé Respiratoire au Cameroun (GESRC). Perennial aeroallergens sensitisation and risk of asthma in African children and adolescents: a case-control study[J].
Asthma,2015, 52 (6) : 57.
(0)
|
| [35] |
Patelis A, Dosanjh A, Gunnbjrnsdottir M, et al. New data analysis in a population study raises the hypothesis that particle size contributes to the pro-asthmatic potential of small pet animal allergens[J].
Ups J Med Sci,2015, 26 : 1-8.
(0)
|
| [36] |
程雷, 毛晓全, 徐其昌. 变应性鼻炎发病与空气污染饮食和感染的关系[J].
中华耳鼻咽喉头颈外科杂志,2003, 38 (1) : 71-73.
(0)
|
| [37] |
Julia V, Macia L, Dombrowicz D. The impact of diet on asthma and allergic diseases[J].
Nat Rev Immunol,2015, 15 (5) : 308-322.
(0)
|
| [38] |
顾之燕. 饮食中缺乏抗氧化剂是呼吸道变应性疾病流行的危险因素之一[J].
中华耳鼻咽喉头颈外科杂志,2008, 43 (1) : 5-6.
(0)
|
| [39] |
Tamay Z, Akcay A, Ergin A, et al. Effects of dietary habits and risk factors on allergic rhinitis prevalence among Turkish adolescents[J].
Int J Pediatr Otorhinolaryngol,2013, 77 (9) : 1416-1423.
(0)
|
| [40] |
Tamay Z, Akcay A, Ergin A, et al. Dietary habits and prevalence of allergic rhinitis in 6 to 7-year-old schoolchildren in Turkey[J].
Allergol Int,2014, 63 (4) : 553-562.
(0)
|
| [41] |
Hao N, Whitelaw M L. The emerging roles of AhR in physiology and immunity[J].
Biochem Pharmacol,2013, 86 (5) : 561-570.
(0)
|
| [42] |
Nguyen N T, Hanieh H, Nakahama T, et al. The roles of aryl hydrocarbon receptor in immune responses[J].
Int Immunol,2013, 25 (6) : 335-343.
(0)
|
| [43] |
Hao N, Whitelaw M L. The emerging roles of AhR in physiology and immunity[J].
Biochem Pharmacol,2013, 86 (5) : 561-570.
(0)
|
| [44] |
Zhou Y, Mirza S, Xu T, et al. Aryl hydrocarbon receptor (AhR) modulates cockroach allergen-induced immune responses through active TGFβ1 release[J].
Mediators Inflamm,2014, 591479 .
doi: 10.1155/2014/591479.Epub2014Mar26 (0)
|
| [45] |
Wei P, Hu G H, Kang H Y, et al. Increased aryl hydrocarbon receptor expression in patients with allergic rhinitis[J].
QJM,2014, 107 (2) : 107-113.
(0)
|
| [46] |
Veldhoen M, Hirota K, Westendorf A M, et al. The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins[J].
Nature,2008, 453 (7191) : 106-109.
(0)
|
| [47] |
Quintana F J, Basso A S, Iglesias A H, et al. Control of T(reg) and T(H)17 cell differentiation by the aryl hydrocarbon receptor[J].
Nature,2008, 453 (7191) : 65-71.
(0)
|
| [48] |
Sim C S, Lee J H, Kim S H, et al. Oxidative stress in schoolchildren with allergic rhinitis: propensity score matching case-control study[J].
Ann Allergy Asthma Immunol,2015, 115 (5) : 391-395.
(0)
|
| [49] |
Ling Y, Yin-Shi G, Hong-Wei S, et al. Oxidative stress status in umbilical cord blood from neonates born to mothers with atopic asthma[J].
Matern Fetal Neonatal Med,2014, 27 (2) : 192-196.
(0)
|
| [50] |
Jiang L, Diaz P T, Best T M, et al. Molecular characterization of redox mechanisms in allergic asthma[J].
Ann Allergy Asthma Immunol,2014, 113 (2) : 137-142.
(0)
|
| [51] |
Comhair S A, Erzurum S C. Redox control of asthma: molecular mechanisms and therapeutic opportunities[J].
Antioxid Redox Signal,2010, 12 (1) : 93-124.
(0)
|
| [52] |
Rahman I, Adcock I M. Oxidative stress and redox regulation of lung inflammation in COPD[J].
Eur Respir J,2006, 28 (1) : 219-242.
(0)
|
| [53] |
Carvalho H, Evelson P, Sigaud S, et al. Mitogen-activated protein kinases modulate H(2)O(2)-induced apoptosis in primary rat alveolar epithelial cells[J].
Cell Biochem,2004, 92 (3) : 502-513.
(0)
|
| [54] |
Kohli A, Garcia M A, Miller R L, et al. Secondhand smoke in combination with ambient air pollution exposure is associated with increasedx CpG methylation and decreased expression of IFN-gamma in T effector cells and Foxp3 in T regulatory cells in children[J].
Clin Epigenetics,2012, 4 (1) : 17.
(0)
|
| [55] |
Adenuga D, Yao H, March T H, et al. Histone deacetylase 2 is phosphorylated,ubiquitinated,and degraded by cigarette smoke[J].
Am J Respir Cell Mol Biol,2009, 40 (4) : 464-473.
(0)
|
| [56] |
Liu J, Ballaney M, Al-alem U, et al. Combined inhaled diesel exhaust particles and allergen exposure alter methylation of T helper genes and IgE production in vivo[J].
Toxicol Sci,2008, 102 : 76-81.
(0)
|
| [57] |
Sofer T, Baccarelli A, Cantone L, et al. Exposure to airborne particulate matter is associated with methylation pattern in the asthma pathway[J].
Epigenomics,2013, 5 (2) : 147-154.
(0)
|
| [58] |
Yang I V, Pedersen B S, Liu A, et al. DNA methylation and childhood asthma in the inner city[J].
Allergy Clin Immunol,2015, 136 (1) : 69-80.
(0)
|
| [59] |
Feng Y, Kong Y, Barnes P F, et al. Exposure to cigarette smoke inhibits the pulmonary T-cell response to influenza virus and Mycobacterium tuberculosis[J].
Infect Immun,2011, 79 (1) : 229-237.
doi: 10.1128/IAI.00709-10 (0)
|
| [60] |
Suen J L, Hsu S H, Hung C H, et al. A common environmental pollutant,4-nonylphenol,promotes allergic lung inflammation in a murine model of asthma[J].
Allergy,2013, 68 (6) : 780-787.
(0)
|
| [61] |
Lee J Y, Kang S K, Heo Y J, et al. Influence of flaxseed oil on fecal microbiota,egg quality and fatty acid composition of egg yolks in laying hens[J].
Curr Microbiol,2016, 72 (3) : 259-66.
doi: 10.1007/s00284-015-0946-z (0)
|
| [62] |
Lyte M, Chapel A, Lyte J M, et al. Resistant Starch Alters the Microbiota-Gut Brain Axis: Implications for Dietary Modulation of Behavior[J].
PLoS One,2016, 11 (1) : e0146406.
(0)
|
| [63] |
Williams B A, Zhang D, Lisle A T, et al. Soluble arabinoxylan enhances large intestinal microbial health biomarkers in pigs fed a red meat-containing diet[J].
Nutrition,2016, 32 (4) : 491-497.
doi: 10.1016/j.nut.2015.10.008 (0)
|
| [64] |
Shandilya U K, Sharma A, Kapila R, et al. Probiotic Dahi containing Lactobacillus acidophilus and Bifidobacterium bifidum modulatesimmunoglobulin levels and cytokines expression in whey proteins sensitized mice[J].
J Sci Food Agric,2015 .
doi: 10.1002/jsfa.7497. (0)
|
| [65] |
张清照, 嶋田貴志, 程雷. 肠球菌属益生菌提取物LFK对变应性鼻炎小鼠血清IL-12的影响[J].
山东大学耳鼻喉眼学报,2014, 28 (3) : 7-9.
(0)
|
| [66] |
朱鲁平, 张清照, 嶋田貴志, 等. 肠球菌属益生菌对实验性变应性鼻炎的抗变态反应作用研究[J].
中华耳鼻咽喉头颈外科杂志,2013, 48 (7) : 555-562.
ZHU Luping, ZHANG Qingzhao, SHIMADA Takashi, et al. Anti-allergic effects of the probiotic preparations of Enterococcus on experimental allergic rhinitis in mice[J]. Chin J Otorhinolaryngol Head Neck Surgery,2013, 48 (7) : 555-562. ( 0)
|
| [67] |
Takeda K, Suzuki T, Shimada S I, et al. Interleukin-12 is involved in the enhancement of human natural killer cell activity by Lactobacillus casei Shirota[J].
Clin Exp Immunol,2006, 146 (1) : 109-115.
(0)
|
| [68] |
Kwon H K, Lee C G, So J S, et al. Generation of regulatory dendritic cells and CD4+ Foxp3+ T cells by probiotics administration suppresses immune disorders[J].
Proc Natl Acad Sci USA,2010, 107 (5) : 2159-2164.
(0)
|