脂溢性皮炎患者血清中抗马拉色菌抗体检测

为了探讨马拉色菌在脂溢性皮炎发病中的作用和意义,我们采用病例对照设计,以马拉色菌(原卵形糠秕孢子菌P.ovale)整菌(WPO)、胞外提取物(ECE)、胞壁提取物(CWE)、胞浆提取物(CPE)为抗原,用间接酶联免疫吸附试验(ELISA)方法检测37例脂溢性皮炎患者和正常人血清中的抗P.ovale抗体。脂溢性皮炎患者血清中抗WPO和抗CPEIgG抗体高于正常对照组(P<0.01),其平均OD值约为正常对照组的1.6～1.8倍,而抗ECE、CWEIgG抗体与正常对照组差异无显著性(P>0.05);4个抗原的IgASD均有不同程度上升,上升明显且具有统计学意义的是抗ECE、CPE的IgA(P<0.01,P<0.05);除抗WPOIgM升高外,余IgM抗体均有不同程度的下降。结果提示脂溢性皮炎的发病可能与马拉色菌相关,脂溢性皮炎患者可能存在某些分子水平上免疫调节方面的缺陷。     

头皮屑和头皮脂溢性皮炎患者头皮脂类水平及马拉色菌数量的检测

目的:测定有头皮屑及头皮脂溢性皮炎患者与正常受试者头皮表面脂类水平及马拉色菌数量的差异。方法:使用sebumeter于洗发后连续4天测量受试者额、顶、枕部头皮皮脂,并于第4天真菌镜检马拉色菌,记录马拉色菌数量。结果:有头皮屑及头皮脂溢性皮炎组与正常对照组相比,马拉色菌数量显著增高,具有统计学意义(P<0.05)。头皮脂溢性皮炎组较头皮屑组的马拉色菌数量显著增高,具有统计学意义(P<0.05)。在头皮屑及头皮脂溢性皮炎组中,随着炎症程度加重,检出的马拉色菌孢子数增多。结论:马拉色菌感染可能与头皮屑多和脂溢性皮炎有关。     

脂溢性皮炎不是由对糠秕马拉色菌的免疫改变应答所致

脂溢性皮炎(SD)是一种常见病,临床有证据支持该病与糠秕马拉色菌显著相关,又因SD患者在HIV感染者中更多见,所以提出了免疫缺陷可能导致SD的假说。先前的一些对SD免疫系统的研究结果有许多争议,现从对糠秕马拉色菌免疫反应的测定来说明免疫反应的改     

糠秕马拉色菌相关皮肤病的免疫学研究现状

糠秕马拉色菌为人体皮肤正常菌群(亦为条件致病菌)之一,与之相关的皮肤疾病有:花斑癣、糠秕马拉色茁毛囊炎(原糠秕孢子菌毛囊炎)、脂溢性皮炎、特应性皮炎和银屑病等。对糠秕马拉色菌和与之相关的主要皮肤病的免疫学研究进行了综述,并对今后的研究设计和研究方法进行了展望。     

花斑癣及脂溢性皮炎患者对糠秕马拉色菌的体液免疫反应

糠秕马拉色菌为一种依赖脂质的双相真菌,按其酵母形态的不同分为卵圆型糠秕孢子菌(芽孢颈部宽的)、圆型糠秕孢子菌(芽孢颈部窄的)及椭圆型糠秕孢子菌。此外,糠秕马拉色菌还可分为7个不同的种。 糠秕马拉色菌既可与皮肤共生,亦可与多种皮肤病及系统性疾病有关,花斑癣、毛囊炎、脂溢性皮炎、异位性皮炎、银屑病及插管所致的系统感染。但其是否可致机体的免疫反应尚有     

金黄色葡萄球菌肠毒素B对特应性皮炎患者外周血细胞因子的影响

目的:初步探讨特应性皮炎(AD)患者外周血单个核细胞(PBMC)Th1、Th2的状态及超抗原的致病机制。方法:分别用金黄色葡萄球菌(金葡菌)肠毒素B(SEB)和植物凝血素(PHA)刺激体外培养的AD患者及健康对照组PBMC,双抗体夹心ELISA法检测PBMC产生的白介素(IL)-4、干扰素(IFN)-γ的含量。结果:PHA刺激后,AD患者PBMC产生的IFN-γ明显低于健康对照组(P<0.01),而两组间IL-4水平差异无显著性(P>0.05);SEB刺激后,AD患者PBMC产生的IL-4水平比健康对照组明显增高(P<0.01),IFN-γ水平明显降低(P<0.01)。结论:AD患者PBMC经SEB刺激后,Th2、Th1细胞亚群失衡,表现为Th2细胞亚群呈优势表达。     

糠秕马拉色菌感染与寻常性银屑病患者血清炎性因子的关系研究

目的探讨糠秕马拉色菌抗体与寻常性银屑病患者血清炎性因子的关系。方法 2014年5月—2015年12月分别应用ELISA法测定68例寻常性银屑病患者及35例正常健康体检者(对照组)血清中抗糠秕马拉色菌可溶性抗原(Sag)、整菌抗原(Wag)Ig G、Ig A、Ig M水平及血清白细胞介素-8(IL-8)、肿瘤坏死因子(TNF)-α、P物质(SP)水平。应用Pearson单因素分析糠秕马拉色菌抗原与寻常性银屑病患者血清炎性因子的关系。结果寻常性银屑病进展组、寻常性银屑缓解组、对照组Wag Ig G水平分别为0.563±0.122、0.412±0.121、0.312±0.112,水平依次降低,组间差异均有统计学意义(P0.05);寻常性银屑进展组、寻常性银屑缓解组抗Sag Ig M水平分别为0.098±0.012、0.096±0.010(P0.05),均高于对照组抗Sag Ig M水平(0.145±0.082),差异有统计学意义(P0.05)。寻常性银屑进展组IL-8(256.36±48.25)、TNF-α(18.22±3.25)及SP(312.85±32.56),寻常性银屑缓解组IL-8(128.96±32.52)、TNF-α(7.98±2.45)及SP(285.69±30.48)及对照组IL-8、TNF-α及SP均依次降低,组间差异均有统计学意义(P0.05);糠秕马拉色菌抗体与寻常性银屑患者血清炎性因子相关性分析,抗Wag Ig G水平与IL-8(r=0.325)、TNF-α(r=0.318)、SP(r=0.332)均呈正相关(P0.05);抗Sag Ig M水平与血清IL-8(r=0.345)、TNF-α(r=0.326)、SP(r=0.337)均呈正相关(P0.05)。结论糠秕马拉色菌感染可能与寻常性银屑病的发病有密切的关系,其作用机制可能与糠秕马拉色菌感染后引起体液免疫异常,促使机体炎性因子释放,使得炎性因子在皮损部位大量浓集有关。     

糠秕马拉色菌对活体皮肤等同物的定植

糠秕马拉色菌属(Malassezia)主要为一些亲脂性的双相酵母菌,生长于人类皮肤的角质层,与皮肤表面存在的三酸甘油酯、游离脂肪酸等脂质及皮脂腺有关,能引起花斑癣和脂溢性皮炎,但至今对于它们的侵袭方式及感染过程还了解不多。作者应用活体皮肤等同物(LSE)研究糠秕马拉色菌早期的定植和酵母到菌丝相的转换。即将糠秕马拉色菌(M.furfur)培养于人类角朊细胞上,而后者则置于液态真皮等同     

糠秕孢子菌感染的研究进展

糠秕孢子菌又称糠秕马拉色菌，为嗜脂的腐物寄生性酵母，作为条件致病菌，与它有关的疾病有，花斑癣，脂溢性皮炎，糠秕孢子菌性毛囊炎，某些异位性皮炎，糠秕孢子菌性真菌血症，新生儿脓疱病，甲真菌病及银屑病，就以上疾病的诊疗以及与Ｍ．ｆｕｒｆｕｒ的关系作一综述。     

婴儿头面部脂溢性皮炎马拉色菌带菌情况分析

目的了解患头面部脂溢性皮炎的婴儿与正常婴儿头面部马拉色菌带菌情况及来源分析。方法采用胶带法粘取脂溢性皮炎患儿头面部皮损及其母亲胸前皮肤、正常婴儿额部皮肤及其母亲胸前皮肤等处鳞屑,接种于含菜籽油培养基进行真菌培养,分离马拉色菌,并用生理生化及形态学方法鉴定菌种。结果①4组150例标本中共分离出101株马拉色菌;②脂溢性皮炎患儿与正常婴儿马拉色菌培养阳性率以及菌种构成差异均无显著性意义;③脂溢性皮炎患儿与正常婴儿分别与其母亲的马拉色菌培养阳性率以及菌种构成比较差异均无显著性意义,菌种存在一致性,但一致性较差。结论马拉色菌是患儿皮肤的常驻菌;脂溢性皮炎患儿及正常婴儿皮肤马拉色菌可能部分来源于母亲。     

白介素-19、20和24与银屑病的关系

白介素-19、20和24是新近发现的3种细胞因子，生物功能尚不完全明了，结构上与白介素-10有很高的同源性。相应的受体和基因结构也明显关联，它们及其受体在结构上有同源性，功能上有联系，但又有各自的独特陛。初步研究显示，它们主要分布在银屑病皮损的表皮，在银屑病炎症中发挥重要作用。     

IL-12 and IL-23 affect photocarcinogenesis differently

Induction of DNA damage by UVR is the key event in photocarcinogenesis. IL-12 and IL-23 are related heterodimeric cytokines consisting of a common p40 unit and a p35/IL-12 and a p19/IL-23 chain, respectively. Both exert immunomodulatory activities but are also found to reduce UVR-induced DNA damage presumably via induction of DNA repair. As both cytokines are also produced in the skin, they may mitigate the risk to develop UVR-induced skin cancer. This appears to be the case as mice lacking p40 were previously shown to be at higher risk for skin tumors upon chronic UVR exposure. As these mice express neither IL-12 nor IL-23, the individual effects of IL-12 or IL-23 could not be evaluated. Thus, mice lacking p35 (IL-12p35-/-) or p19 (IL-23p19-/-) were subjected to chronic UVR exposure. The Kaplan-Meier analysis indicated a significantly increased probability of tumor development in IL-23p19-/- but not in IL-12p35-/- mice. Taken together, in our model, loss of IL-23, but not of IL-12, enhances development of UVR-induced skin tumors, indicating that IL-23 but not IL-12 may counteract photocarcinogenesis. This may have impact on the development of future strategies utilizing antibodies against IL-12 and IL-23, respectively, for the treatment of inflammatory dermatoses.     

产妇宫内感染对早产儿IL-1β、IL-6、IL-8、IL-10和TNF-α影响情况研究

目的:探讨产妇宫内感染对早产儿IL-1β、IL-6、IL-8、IL-10和TNF-α的影响。方法:回顾性分析2015年8月至2016年10月在我院接受分娩的宫内感染产妇的早产儿的临床资料,同时选取同期在我院分娩的非宫内感染产妇的早产儿作为对照。观察两组早产儿血清炎症因子水平、NIHSS评分、肾功能、心肌酶指标和出生时一般情况的差异。结果:宫内感染组早产儿的IL-1β、IL-6、IL-8、IL-10和TNF-α水平均高于对照组(t=7.044、12.208、7.289、20.185、5.421,P0.001);宫内感染组早产儿的Sp O2、Pa O2低于对照组(t=-6.353、-35.142,P0.001),Pa CO2水平高于对照组(t=35.720,P0.001);宫内感染组早产儿的NIHSS评分高于对照组(t=50.424,P0.001),出生1min和5min的Apgar评分低于对照组(t=-3.475、-4.398,P0.001);宫内感染组早产儿的尿素氮、肌酐和CK-MB水平均高于对照组(t=49.014、11.611、16.458,P0.001);Pearson相关分析法结果显示,宫内感染早产儿血清IL-1β、IL-6、IL-8、IL-10和TNF-α水平与NIHSS评分、肾功能、心肌酶指标水平正相关,与Apgar评分负相关。结论:宫内感染产妇分娩的早产儿的血IL-1β、IL-6、IL-8、IL-10和TNF-α水平较高,且与患儿的NIHSS评分、肾功能、心肌酶指标密切相关。     

IL-17和IL-23拮抗剂治疗银屑病的研究进展

目前美国食品药品监督局（FDA）批准用于临床的IL-17抗体拮抗剂包括secukinumab、ixekizumab和brodalumab,三者治疗中度至重度斑块状银屑病皮损清除均优于对照组TNF-α拮抗剂,且安全性及耐受性均较好。三种IL-23拮抗剂risankizumab,guselkumab和tildrakizumab目前均在III期临床试验中,初步临床试验结果表明三种药物治疗银屑病较对照组TNF-α拮抗剂具有更快达到皮疹改善、更高皮疹清除率和注射次数更少的优势。本文就上述六种生物制剂治疗银屑病的研究进展进行了综述。     

Role of fibroblasts in the regulation of proinflammatory interleukin IL-1, IL-6 and IL-8 levels induced by keratinocyte-derived IL-1

Received: 15 May 1995     

Th17细胞相关因子与寻常性进行期银屑病的相关性研究

目的探讨Th17细胞相关因子白细胞介素(IL)-17A、IL-17F、IL-21、IL-22与寻常性进行期银屑病发病的相关性。方法通过实时定量反转录聚合酶链式反应(RT-PCR)分别检测30例患者和20名正常人外周血单个核细胞(PBMC)、12例患者皮损、12名正常皮肤组织中上述4种细胞因子的mRNA表达水平。结果患者组PBMC中IL-17A、IL-17F、IL-21和IL-22的mRNA表达水平较正常组显著升高(P均0.05),患者组皮损中4种细胞因子的mRNA表达明显高于正常组(P均0.05)。结论 Th17细胞因子IL-17A、IL-17F、IL-21和IL-22的mRNA水平在患者组PBMC及皮肤组织中明显升高,提示Th17细胞因子可能与寻常性银屑病的发病有一定相关性。     

IL-23-mediated epidermal hyperplasia is dependent on IL-6

Psoriasis is a chronic inflammatory skin disease primarily driven by Th17 cells. IL-23 facilitates the differentiation and induces complete maturation of Th17 cells. Lesional psoriatic skin has increased levels of IL-23 and recent studies show that intradermal injections of IL-23 induce a psoriasis-like skin phenotype in mice. We have now characterized the IL-23-induced skin inflammation in mice at the molecular level and found a significant correlation with the gene expression profile from lesional psoriatic skin. As observed in psoriasis, the pathogenesis of the IL-23-induced skin inflammation in mice is driven by Th17 cells. We demonstrate a dramatic upregulation of IL-6 mRNA and protein after intradermal injections of IL-23 in mice. Using IL-6(-/-) mice we show that IL-6 is essential for development of the IL-23-elicited responses. Despite producing high levels of IL-22, IL-6(-/-) mice were unable to express the high-affinity IL-22 receptor chain and produced minimal IL-17A in response to intradermal injections of IL-23. In conclusion, we provide evidence for the critical role played by IL-6 in IL-23-induced skin inflammation and show that IL-6 is required for expression of IL-22R1A.     

Type I IL-1 receptor mediates IL-1 and intracellular IL-1 receptor antagonist effects in skin inflammation

The IL-1 system plays a key role in skin physiology and pathology. In this study, we used mutant mice lacking the type I IL-1 receptor (IL-1RI), lacking IL-1 receptor antagonist (IL-1Ra), or overexpressing the human intracellular (ic) IL-1Ra1 isoform, as well as combinations thereof, to dissect the role of the IL-1 system in phorbol 13-myristate 12-acetate (PMA)-induced skin inflammation. In wild-type (WT) mice, PMA application induced epidermal thickening and dermal inflammation. Skin IL-1alpha production and circulating levels of the acute-phase protein serum amyloid A (SAA) were elevated. In mice lacking IL-1RI or overexpressing icIL-1Ra1, PMA induced similar epidermal thickening as in WT mice, but dermal inflammation was partially prevented. Skin IL-1alpha mRNA expression was similar in PMA-treated IL-1RI-/- and WT mice, whereas the increase in serum SAA was suppressed in IL-1RI-/- mice. Interestingly, PMA-induced IL-1alpha mRNA expression was further enhanced by icIL-1Ra1 overexpression in an IL-1RI-dependent manner. Finally, IL-1Ra-/- mice spontaneously displayed skin lesions characterized by high IL-1beta, but not IL-1alpha, expression. In conclusion, PMA-induced epidermal thickening and skin IL-1alpha expression were independent of IL-1 signaling, in contrast to dermal inflammation and systemic inflammatory response.     

Histamine-induced IL-6 and IL-8 production are differentially modulated by IFN-gamma and IL-4 in human keratinocytes

It is known that large amounts of histamine are stored in mast cells located in the superficial dermis of the skin and can be released upon appropriate stimulation. However, the effects of histamine on keratinocyte function have not been well characterized. We therefore examined the capacity of histamine to modulate the production of interleukin (IL)-6 and IL-8 by keratinocytes. We found that histamine significantly augmented the production of IL-6 and IL-8 in a dose- and time-dependent manner. The enhancing effects of histamine were completely inhibited by a potent H1 receptor (H1R) antagonist, emedastine difumarate. Pyrilamine (a much weaker H1R antagonist) and cimetidine (an H2R antagonist) only partially inhibited the enhancing effects of histamine. The histamine-induced up-regulation of IL-6 and IL-8 production, however, was completely abrogated by a combination of pyrilamine and cimetidine. The IL-6 production was significantly enhanced by interferon (IFN)-gamma. Interestingly, IFN-gamma and IL-4 both significantly augmented the histamine-induced IL-6 production. On the other hand, the production of IL-8 was inhibited by IFN-gamma, and IFN-gamma and IL-4 both completely abrogated the histamine-induced IL-8 production. These results suggest that the histamine-induced IL-6 production and IL-8 production are differentially regulated by IFN-gamma and IL-4. Histamine may be an important modulator of cytokine production in epidermal milieu.