首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到19条相似文献,搜索用时 31 毫秒
1.
特应性皮炎(atopic dermatitis, AD)是一种以反复发作和严重瘙痒为特征、发病率最高的过敏性皮肤病。AD的致病机制涉及遗传易感性、表皮屏障功能障碍、微生物组失调、免疫反应失衡以及环境等多个因素,而现有治疗用药副作用大、疗效欠佳。目前研究已发现肠道菌群尤其是益生菌在AD中起着重要作用。益生菌能够通过抑制病原菌、增强屏障功能、改善肠道环境和平衡Th1/Th2免疫应答等机制改善AD症状。本文综述了AD患者皮肤及肠道微生态特征,基于AD发病的致病机制和影响因素,系统阐明益生菌缓解AD的机制,以期为益生菌治疗AD及相关皮肤过敏性疾病提供理论支持。  相似文献   

2.
特应性皮炎(atopic dermatitis,AD)是儿童常见的皮肤过敏性疾病,虽然临床表现多样,但基本特征是全身皮肤干燥、慢性湿疹样损害和剧烈瘙痒表现[1]。近十年余中国儿童的AD患病率显着提高,2002年顾恒等[2]对中国的10个城市进行学龄前儿童特应性皮炎现况调查,研究结果发现学龄前儿童AD患病率为2.78%,而在2014年一项对中国12个城市的流行病学调查中发现AD则已影响了30.48%的婴儿以及12.94%的幼儿与学龄前儿童[3-4]。  相似文献   

3.
杨明  刘晓雁  殷妍  黄小兰 《中国微生态学杂志》2021,33(12):1441-1444, 1449
目的 探讨益生菌辅助治疗对儿童中重度特应性皮炎(AD)的临床疗效。 方法 选择于首都儿科研究所附属儿童医院皮肤科就诊的96例中重度AD患儿为研究对象。入选患儿随机分成两组,其中试验组(50例)患儿给予口服乳杆菌及我院皮肤科AD常规药(口服抗组胺药,外用糠酸莫米松乳膏、我院自制肤乐霜);对照组(46例)患儿仅给予我院皮肤科AD常规药。两组患儿均治疗3个月,治疗前后分别用SCORAD评分、CDLQI评分、DFIQ评分进行病情评估,同时检测两组患儿治疗前后的血清总IgE、IL2受体、IL4、嗜酸细胞阳离子蛋白(ECP)水平及Th1/Th2比值。 结果 治疗后,SCORAD评分显示实验组患儿总有效率为82.0%(41/50),对照组总有效率为52.2%(24/46),两者差异有统计学意义(χ2=6.448,P=0.011)。治疗后,试验组患儿SCORAD评分、CDLQI评分、DFIQ、总IgE水平低于对照组(t=4.656,4.189,3.097、2.278;P0.05)。 结论 中重度AD患儿在常规治疗上基础上补充益生菌,可显著降低血清IgE水平,减轻AD患儿的症状,提高疗效。  相似文献   

4.

人类皮肤作为抵御外界病原体入侵的第一道防线,寄居着许多参与防御和免疫反应的微生物,这些微生物帮助维持皮肤健康。特应性皮炎是一种慢性、复发性和炎症性疾病,以皮肤干燥、湿疹样皮炎和瘙痒为主要特征,与皮肤微生态的失衡密切相关。当前,特应性皮炎的治疗主要以抗炎、止痒、调节免疫和提高生活质量为主。“肠道−皮肤轴”的概念提示肠道微生态与皮肤微生态密切相关,揭示调节肠道菌群可能有助于特应性皮炎的治疗。因此,研究皮肤微生态与特应性皮炎的关系,有助于我们深入理解二者之间的相互影响,并为特应性皮炎的诊断和治疗提供新的思路。

  相似文献   

5.
目的系统评价益生菌对婴儿期特应性皮炎的预防作用。方法计算机检索中英文数据库,检索时限从建库到2017年12月,收集益生菌对婴儿期特应性皮炎预防的临床随机对照试验的文献,由2名研究员筛选文献及质量评价,采用RevMan 5.3软件进行Meta分析。结果最终纳入质量较高的20个研究,共3 701例患儿。结果显示:益生菌组特应性皮炎发生率低于对照组,两组差异具有统计学意义(RR=0.74,95%CI:0.64~0.86,P0.01)。进一步亚组分析后发现仅产前母亲或产后婴儿口服益生菌对婴儿期特应性皮炎无预防作用(RR=0.91,95%CI:0.62~1.33,P=0.62;RR=0.91,95%CI:0.71~1.16,P=0.43),而在两者均服用益生菌的比较中发现单独服用乳酸菌类或与其他益生菌混合服用同安慰剂组比较均具有预防作用(RR=0.70,95%CI:0.52~0.94,P0.05;RR=0.65,95%CI:0.50~0.86,P0.01)。结论孕母及产后婴儿均补充益生菌对婴儿期特应性皮炎具有预防作用,单独服用临床常用的乳酸菌类或与其他益生菌混合服用同样具有保护作用,但由于国内外菌株、种群差异等诸多因素,其对婴儿期特应性皮炎的保护机制在国内尚需进一步研究。  相似文献   

6.

肠道微生物群是定植于人类肠道内的微生物群体,包括细菌、真菌和病毒等。普拉梭菌是一种常见的肠道细菌,在维持肠道菌群平衡和人体免疫系统中发挥重要作用。特应性皮炎是一种慢性炎症性皮肤病,肠道菌群失调与特应性皮炎的发生和发展有关。普拉梭菌作为肠道菌群的重要成员,其变化会导致特应性皮炎患者的免疫反应紊乱和皮肤炎症加重。近年来利用普拉梭菌治疗特应性皮炎的研究还处于动物研究阶段,未来的研究应进一步揭示普拉梭菌与特应性皮炎之间的复杂关系,并为治疗特应性皮炎开发新的策略提供有益的见解。

  相似文献   

7.
胡笑笑  田晔 《中国微生态学杂志》2022,(11):1338-1341+1347
皮肤和人体微生物群相互作用,关系复杂。特应性皮炎(atopic dermatitis,AD)是一种常见的慢性和易复发性疾病,与机体的内部和外部环境相关,发病率呈上升趋势。AD的发生往往会改变人体微生物群的组成和数量,微生物群的定植在AD的发生和发展中起着主要作用。本文就人体微生物群与AD的关系、基于皮肤微生物群的AD研究及基于肠道微生物群的AD研究三方面进行综述,主要阐述了皮肤微生物群和肠道微生物群与AD的关系,重点讨论金黄色葡萄球菌在AD发生中的作用以及益生菌等微生物在AD治疗中的重要作用,以期为AD的防治提供新的思路。  相似文献   

8.

特应性皮炎(atopic dermatitis, AD)是一种常见的慢性炎症性皮肤病, 可发生于各个年龄段, 婴幼儿尤为高发。AD病因复杂, 既往认为遗传背景、皮肤屏障功能障碍和免疫紊乱是其主要发病机制。近年来皮肤微生态在AD发病中的作用被逐渐揭示, 成人AD常伴有以金黄色葡萄球菌定植增加和菌群多样性下降为主要特征的皮肤菌群失调。婴幼儿皮肤屏障功能与免疫功能随着年龄增长发生显著变化, 其皮肤菌群特点也不同于成人, 国内对此领域关注较少, 因此本文就婴幼儿皮肤微生态的特点及其在AD发病中的作用作一综述。

  相似文献   

9.
近年来,对马拉色菌与免疫系统之间关联的研究明显增加,其重要内容是马拉色菌在特应性皮炎发病中的作用。本文主要概述近期一些研究中对马拉色菌与树突状细胞、角质形成细胞间的关联性及其在特应性皮炎发病的免疫学机制中的作用所获得的进展。  相似文献   

10.
摘要 目的:分析不同严重程度儿童特应性皮炎血清半乳糖凝集素-10(Gal-10)及炎症因子的表达水平及其与皮肤感染的相关性。方法:选择我院自2022年1月至2023年1月收治的110例特应性皮炎患儿纳入观察组,根据特应性皮炎评分(SCORAD),分为轻度组、中度组和重度组;另选110例健康体检儿童纳入对照组。检测所有入选者血清Gal-10、炎症因子(IL-4、IL-13、IL-31)水平及不同部位皮肤经皮失水量,分析血清Gal-10、IL-4、IL-13、IL-31与SCORAD评分、不同部位皮肤经皮失水量的关系,使用受试者工作特征曲线(ROC)分析血清Gal-10、炎症因子(IL-4、IL-13、IL-31)对皮肤感染的预测效能。结果:观察组血清Gal-10、IL-4、IL-13、IL-31水平均高于对照组(P<0.05);随着儿童特应性皮炎病情加重,患儿血清Gal-10、IL-4、IL-13、IL-31水平随之升高,血清Gal-10、IL-4、IL-13、IL-31水平在轻度组、中度组和重度组中差异显著(P<0.05);经Pearson相关性分析,特应性皮炎患儿血清Gal-10、IL-4、IL-13、IL-31水平与SCORAD评分,前壁伸侧、前壁屈侧、脸颊及胫前的经皮失水量呈正相关(P<0.05);在110例特应性皮炎患儿中,发生皮肤感染43例;经ROC曲线分析,血清Gal-10、IL-4、IL-13联合IL-31预测特应性皮炎患儿发生皮肤感染的敏感度为89.72%、特异度为56.97%、ROC曲线下面积(AUC)为0.921。结论:血清Gal-10、炎症因子(IL-4、IL-13、IL-31)水平与儿童特应性皮炎严重程度有显著相关性,对于评估其皮肤屏障功能和预测皮肤感染均具有一定作用,值得临床予以重视应用。  相似文献   

11.
Patients with atopic dermatitis (AD) are highly susceptible to viral, bacterial, and fungal skin infections because their skin is dry and this compromises the barrier function of the skin. Therefore, the skin microbiota of patients with AD is believed to be different from that of healthy individuals. In the present study, the skin fungal microbiota of nine patients with mild, moderate, or severe AD and ten healthy subjects were compared using an rRNA clone library. Fungal D1/D2 large subunit analysis of 3647 clones identified 58 species and seven unknown phylotypes in face scale samples from patients with AD and healthy subjects. Malassezia species were predominant, accounting for 63%-86% of the clones identified from each subject. Overall, the non-Malassezia yeast microbiota of the patients was more diverse than that of the healthy individuals. In the AD samples 13.0 ± 3.0 species per case were detected, as compared to 8.0 ± 1.9 species per case in the samples taken from healthy individuals. Notably, Candida albicans, Cryptococcus diffluens, and Cryptococcus liquefaciens were detected in the samples from the patients with AD. Of the filamentous fungal microbiota, Cladosporium spp. and Toxicocladosporium irritans were the predominant species in these patients. Many pathogenic fungi, including Meyerozyma guilliermondii (anamorphic name, Candida guilliermondii), and Trichosporon asahii, and allergenic microorganisms such as Alternaria alternata and Aureobasidium pullulans were found on the skin of the healthy subjects. When the fungal microbiota of the samples from patients with mild/moderate to severe AD and healthy individuals were clustered together by principal coordinates analysis they were found to be clustered according to health status.  相似文献   

12.
    
Fibroblast growth factors (FGFs) are key regulators of tissue development, homeostasis and repair, and abnormal FGF signalling is associated with various human diseases. In human and murine epidermis, FGF receptor 3 (FGFR3) activation causes benign skin tumours, but the consequences of FGFR3 deficiency in this tissue have not been determined. Here, we show that FGFR3 in keratinocytes is dispensable for mouse skin development, homeostasis and wound repair. However, the defect in the epidermal barrier and the resulting inflammatory skin disease that develops in mice lacking FGFR1 and FGFR2 in keratinocytes were further aggravated upon additional loss of FGFR3. This caused fibroblast activation and fibrosis in the FGFR1/FGFR2 double‐knockout mice and even more in mice lacking all three FGFRs, revealing functional redundancy of FGFR3 with FGFR1 and FGFR2 for maintaining the epidermal barrier. Taken together, our study demonstrates that FGFR1, FGFR2 and FGFR3 act together to maintain epidermal integrity and cutaneous homeostasis, with FGFR2 being the dominant receptor.  相似文献   

13.
14.
    
Seborrheic dermatitis (SD) is a chronic inflammatory dermatologic condition in which erythema and itching develop on areas of the body with sebaceous glands, such as the scalp, face and chest. The inflammation is evoked directly by oleic acid, which is hydrolyzed from sebum by lipases secreted by skin microorganisms. Although the skin fungal genus, Malassezia, is thought to be the causative agent of SD, analysis of the bacterial microbiota of skin samples of patients with SD is necessary to clarify any association with Malassezia because the skin microbiota comprises diverse bacterial and fungal genera. In the present study, bacterial microbiotas were analyzed at non‐lesional and lesional sites of 24 patients with SD by pyrosequencing and qPCR. Principal coordinate analysis revealed clear separation between the microbiota of non‐lesional and lesional sites. Acinetobacter, Corynebacterium, Staphylococcus, Streptococcus and Propionibacterium were abundant at both sites. Propionibacterium was abundant at non‐lesional sites, whereas Acinetobacter, Staphylococcus and Streptococcus predominated at lesional sites; however, the extent of Propionibacterium colonization did not differ significantly between lesional and non‐lesional sites according to qPCR. Given that these abundant bacteria hydrolyze sebum, they may also contribute to SD development. To the best of our knowledge, this is the first comprehensive analysis of the bacterial microbiotas of the skin of SD patients.  相似文献   

15.
特应性皮炎(atopic dermatitis,AD)是一种难治易复发皮肤病,由于病因复杂且患病率逐年增加,该病已经成为公共卫生领域关注的问题。随着高通量测序、元基因组学和代谢组学等技术的应用,发现AD的发生与发展与微生物群落息息相关,“微生物-皮-肠”轴及它们之间的串扰机制也逐渐被验证。“微生物-皮-肠”轴在过敏性皮肤炎症中扮演了重要角色。本文综述了“微生物-皮-肠”轴与AD的关系,及其可能交流的信号分子和潜在途径,重点关注了涉及益生菌、菌群移植和抗菌肽等微生物缓解AD的潜在机制,为靶向微生物群治疗过敏性皮肤炎症提供了一个新的视角。  相似文献   

16.
    
Fecal microbiota and polyamine concentration obtained from eleven intractable adult-type atopic dermatitis (AD) patients and thirteen healthy adults were compared. Fecal microbiota were analyzed using terminal-restriction fragment length polymorphism. The fecal microbiota of volunteers were divided into two clusters, A (n=16) and B (n=8), and the number of AD patients was found to be higher in Cluster B than Cluster A, suggesting that there are relationships between the obstinacy of intractable adult-type AD and intestinal microbiota in Cluster B. Fecal spermidine concentration in Cluster B were lower than that in Cluster A significantly (P<0.05). Fecal putrescine concentration in Cluster B also tended to be lower than that in Cluster A. Terminal-restriction fragment (T-RF) of 122 bp generated by digestion with Hha I, which were predicted as unknown bacteria, were detected characteristically in Cluster A. In contrast, T-RFs of 368/9 bp generated by digestion with Hha I, which were predicted as Enterobacteriaceae, were detected characteristically in Cluster B. These bacteria are closely associated with intestinal polyamine concentration. These findings raise the possibility that a low concentration of intestinal polyamines produced by intestinal microbiota is one of the important factors in the onset of intractable adult-type AD.  相似文献   

17.
皮肤是人体最大的器官,也是人体第二大微生物群的载体。皮肤是抵御外部刺激的屏障,紫外线、雾霾等外界环境的刺激会造成皮肤损伤,引起皮肤老化或屏障受损。后生元被定义为“赋予宿主健康益处的无生命微生物或其成分的制剂”。近年来的研究表明,后生元在维护皮肤健康方面具有极大潜力。本文介绍了后生元及其类型,阐述了后生元在修复皮肤屏障、促进伤口愈合、抵御皮肤光老化以及调节皮肤微生物群等方面的潜在作用,为后生元在皮肤健康益处的深入研究及原料开发提供参考。  相似文献   

18.
Nodakenin, derived from the roots of Angelica gigas Nakai, is an important natural resource and medicinal material with anti-allergic and anti- inflammatory activities. We have previously shown that nodakenin inhibits IgE/Ag-induced degranulation in mast cells. In this study, we investigated the inhibitory effect of nodakenin on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD)- like skin lesions in ICR mice. Scratching behavior, skin severity score, blood IgE level, and skin thickness were improved in DNCB-induced AD-like ICR mice. Our results showed that nodakenin suppressed the increase of AD-like skin lesions in ICR mice. These results suggest that nodakenin may be a potential therapeutic resource for AD as well as an adjunctive agent to control itching associated with AD.  相似文献   

19.
    
《Cell host & microbe》2022,30(3):301-313.e9
  1. Download : Download high-res image (242KB)
  2. Download : Download full-size image
  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号