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银屑病与真菌感染的关系综述

来源:菌物学报 作者:蓝雨;席丽艳;张军民
发布于:2019-07-19 共10759字

  摘    要: 随着近年来银屑病的发病率逐步增加,关于银屑病病因的研究更加深入。除了遗传、免疫和环境等相关因素,微生物与银屑病的关系也备受关注。关于真菌感染与银屑病的相关性研究始于19世纪,认为糠秕马拉色菌可能是银屑病的致病因子,与银屑病的发生发展密切相关。随后也有研究指出白色念珠菌通过超抗原等作用诱发或加重银屑病。但银屑病患者依据自身IL-17增高的特点可以起到一定抵抗微生物感染的作用,因此真菌感染与银屑病的关系暂无定论。随着近年来关于两者之间的研究逐渐增多,真菌感染仍是银屑病患者不可忽视的诱发或加重因素之一。明确真菌感染在银屑病患者体内的作用有助于更好的研究银屑病的发病机制以及改善预后。

  关键词: 银屑病; 马拉色菌属; 念珠菌属; 真菌; 感染;

  Abstract: With the increasing incidence of psoriasis in recent years, research on the etiology of psoriasis has become deepgoing. The study on the correlation between fungal infection and psoriasis began in the 19th century, and it was believed that malasszia infection might be the pathogenesis of psoriasis, and the fungus was closely related to the occurrence and development of psoriasis. Some studies indicated that candida albicans induced or aggravated psoriasis through superantigen. However, relying on the characteristics of increasing Il-17, psoriasis patients can resist microbial infection to a certain extent. The relationship between fungal infection and psoriasis is not conclusive yet. With the deepening research, fungal infection is still regarded as one of the factors that can not be ignored in inducing or aggravating psoriasis.

  Keyword: psoriasis; Malassezia; Candida; fungi; infection;

  银屑病是一种多因素参与的慢性免疫异常性的炎症性皮肤病,其特征是由T细胞介导的角质形成细胞过度增殖。虽然被认为是自身免疫性相关疾病,但是越来越多证据表明遗传、环境和微生物在疾病的起始和发展中起作用,包括马拉色菌和白色念珠菌等被认为与银屑病的发病关系密切。本文从银屑病病因、发病机理、临床表现与治疗方面综述了银屑病与真菌感染的关系和相互影响。

  1、 皮肤微生物定植异常与银屑病

  正常情况下,人的皮肤被大量微生物定植,微生物以共生的状态附着在皮肤上,下调皮肤的免疫反应而不会引起临床症状。如果病原体在皮肤屏障功能受损的情况下攻击机体,引起皮肤中的各种免疫细胞和免疫因子表达,在病原体侵袭能力强的情况下,马拉色菌等条件致病菌就转变为致病菌。除了常见的花斑癣、脂溢性皮炎等与马拉色菌密切相关之外,头皮及胸背部的银屑病也常合并有马拉色菌感染(Rudramurthy et al. 2014)。在脂溢性皮炎、特应性皮炎和银屑病等炎性皮肤病当中,马拉色菌主要通过产生脂肪酶和磷脂酶破坏表皮屏障功能(Gaitanis et al. 2013)。其中糠秕马拉色菌(Malassezia furfur)可以分泌更多的脂肪酶,促进花生四烯酸及其代谢产物的释放,因此加剧银屑病的炎症反应及过度增殖(Zomorodian et al. 2010)。但糠秕马拉色菌并不一定是银屑病最常见的马拉色菌种属,既往研究报道球形马拉色菌和限制性马拉色菌都常见于银屑病患者(Jagielski et al. 2014;Prohi? et al. 2016)。并且研究发现随着银屑病病情的进展,马拉色菌的种类从限制性马拉色菌逐渐转变成球形马拉色菌(Gomez-Moyano et al. 2014),这可能意味着不同种属致病力的差别。

银屑病与真菌感染的关系综述

  白色念珠菌最主要定植于银屑病患者的口腔内,也常见于潮湿的褶皱部位,如腋窝、臀间以及指甲褶皱处。一项荟萃分析总结了银屑病患者皮肤黏膜念珠菌的发病率,发现其检出率显着高于对照组,尤其在口腔粘膜中(Pietrzak et al. 2018),表示银屑病患者可能是口腔念珠菌感染的易感人群。

  2、 真菌感染与银屑病皮损

  早在20世纪Lober et al.(1982)使用已经灭活的糠秕孢子菌(现已改名为糠秕马拉色菌)悬液在银屑病患者的正常皮肤上进行斑贴试验,发现糠秕孢子菌使该部位皮肤产生红斑鳞屑样改变,并用病理证实了此部位银屑病样改变。另一项早期病例报道(Elewski 1990)描述了某银屑病患者在马拉色菌毛囊炎的部位新发了点滴状的银屑病皮损。上述研究是最初认为真菌感染通过同形反应(Koebner现象)引起银屑病再发。相反,Leibovici et al.(2015)的研究指出银屑病患者的足癣患病率为13.8%,显着高于正常对照组,红色毛癣菌为其最常见的培养真菌,证明了银屑病和真菌感染彼此促进的相互作用。

  甲癣的易感因素除了包括反复的指甲外伤、遗传、糖尿病等因素,指甲形态异常也是甲癣的易感因素之一。银屑病常累及指甲,造成指甲外观改变,甲板从甲床脱离而失去其天然屏障,成为更有利于真菌生长的环境。因此被认为更易合并真菌感染(Runne & Orfanos 1981;Elewski 1998)。希腊的一项横断面研究统计了未使用过免疫抑制剂和/或抗真菌药物的银屑病患者的甲癣发生率,发现其甲癣的患病率为34.78%,高于希腊的一般人群,酵母菌和霉菌是最主要的分离菌(Tsentemeidou et al. 2017)。Rizzo et al.(2013)的一项描述性分析表明,合并甲真菌病的银屑病患者的NAPSI指数高于非甲真菌感染的银屑病甲患者,说明甲真菌感染也可能通过Koebner现象加剧银屑病的发展,导致先前存在的银屑病恶化。

  3、 抗真菌治疗与银屑病

  对于抗真菌药物,既往研究证明酮康唑对头皮难治性银屑病具有良好的治疗效果(Rosenberg & Belew 1982),并不止是单纯抑制马拉色菌生长,还可以通过抑制真菌抗原诱导淋巴细胞介导的免疫反应改善银屑病(Alford et al. 1986)。在亚洲头皮银屑病研究组(ASPSG)的指南上指出酮康唑的额外抗炎作用可能有助于轻度头皮银屑病患者改善病情,并且抗真菌药物可能最适用于脂漏性干癣(sebopsoriasis)迹象的患者或免疫功能低下的患者(Frez et al. 2014)。这证明抗真菌药物在消灭真菌后,同时改善了银屑病皮损的进展。临床研究表明在银屑病患者身上,先使用伊曲康唑减少马拉色菌的数量后,再使用卡泊三醇治疗头皮银屑病,与对照组相比后续使用卡泊三醇的刺激性明显减少。说明马拉色菌的存在不仅恶化了银屑病,还加剧了药物治疗的副作用(Faergemann et al. 2003)。但于此同时,抗真菌药物也可能对银屑病的发展起到反作用。银屑病患者用伊曲康唑治疗甲真菌病的疗效低于一般人群(Shemer et al. 2010),并且更严重的是抗真菌药物的使用可能加重银屑病的发生发展(Le Guyadec et al. 2000;Szepietowski 2003)。Chiu et al.(2018)的研究发现,使用特比萘芬或伊曲康唑可以增加银屑病的风险,并且对于近期的药物接触史其作用更为强烈。这种情况可能是由于伊曲康唑和特比萘芬通过增加前列腺素D2(PGD2)的释放增强角质形成细胞中人β-防御素3(hBD-3)的产生(Kanda et al. 2011),并且激活朗格汉斯细胞,加剧银屑病的皮肤炎症反应(Sweeney et al. 2016)。

  在银屑病治疗相关药物方面,糖皮质激素、免疫抑制剂的使用可以增加真菌感染的发生率。不仅局限于皮肤癣菌的感染,既往研究报道过银屑病患者在接受依那西普治疗后出现头皮白色隐球菌感染(Hoang & Burruss 2007);在依法珠单抗,甲氨蝶呤和环孢素联合治疗后出现的播散性隐球菌感染(Tuxen et al. 2007);以及激素联合环孢素治疗后引起的皮下赛多孢子菌感染,并且在停药后自愈(Li et al. 2017)。目前针对IL-17的生物制剂已广泛使用,这个治疗方法带来不可忽视的副作用就是感染,尤其是与IL-17相关宿主防御机制的念珠菌感染(Saunte et al. 2017)。一项随机前瞻性研究比较了接受依那西普,英夫利昔单抗,阿达木单抗治疗和对照组指甲受累的银屑病患者的甲癣发生风险,发现接受抗TNF-α药物治疗的银屑病甲患者的甲癣发生率为20.3%,而对照组为13.89%。英夫利昔单抗的风险在统计学上显着更高。因此作者得出结论,甲真菌病与接受抗TNF治疗的指甲银屑病患者之间存在显着相关性,尤其是英夫利昔单抗(Al-Mutairi et al. 2013)。

  4、 真菌性细胞增殖与银屑病

  银屑病的临床表现源于表皮角质形成细胞的过度增殖及异常分化,而糠秕马拉色菌与角质形成细胞之间的相互作用对于银屑病的发生发展起到重要作用。糠秕马拉色菌通过细胞内的Toll样受体或Nod样受体信号通路刺激角质形成细胞增殖(Carlo et al. 2012),并且通过附着在炎症性皮肤病如脂溢性皮炎和银屑病上,进而促进上皮细胞更新和剥落,加重原有的炎症反应(Dessinioti & Katsambas 2013)。Baroni et al.(2004)的试验中,发现糠秕马拉色菌通过AP-1依赖性机制上调人角质形成细胞中的转化生长因子-β1(TGF-β1)、整合素链和HSP70的表达,与表皮的过度增殖和细胞迁移相关。与马拉色菌阴性的点滴型银屑病患者相比,马拉色菌阳性的点滴型银屑病患者Th2细胞因子(IL-4,IL-10,IL-13)的平均水平显着降低。作者认为低水平的Th2细胞因子可能促进点滴型银屑病患者的炎症反应和加剧过度增殖状态(Aydogan et al. 2013)。证明了糠秕马拉色菌对于银屑病患者细胞免疫功能的影响。邓国辉和杨国良(2018)通过ELISA 法测定寻常性银屑病(PV)患者和健康对照组血清中抗糠秕马拉色菌可溶性抗原(Sag)、整菌抗原(Wag)IgG,IgA,IgM水平。结果显示PV患者抗Sag IgM水平较健康对照组明显降低,PV患者抗Wag IgG明显高于健康对照组。可能是由于抗Sag IgM水平与抗Wag IgG水平发生交叉作用,导致病原菌细胞免疫发生异常,与银屑病的发病机制相关。

  在过去的几十年中,已经报道了来自微生物包括葡萄球菌,链球菌,白色念珠菌及糠秕马拉色菌的超抗原在银屑病发病机理中的潜在作用(Devore-Carter et al. 2008)。Metin et al.(2015)发现,念珠菌或马拉色菌不仅引起皮肤皱褶部位的感染,而且通过启动特异性体液或细胞免疫应答机制,间接诱发或加重银屑病。超抗原通过HLA-DR抗原呈递细胞呈递给皮肤中的T细胞,诱导机体的特异性细胞免疫应答。激活的T细胞迁徙到表皮并释放炎症介质和细胞因子,促进角质形成细胞的快速增殖,因此促进银屑病的发生发展(Leung et al. 1993)。

  这些临床表现,治疗效果和免疫学结果表明,真菌感染与银屑病的发生发展相互促进。马拉色菌和白色念珠菌可能通过多种机制导致银屑病恶化,并且银屑病本身可能更易合并真菌感染。结合上述研究结果,真菌与银屑病之间相互促进的关系不可否认。临床上对于头皮及褶皱部位的银屑病皮损,完善真菌相关检查,并积极治疗银屑病患者合并的真菌感染,有助于改善银屑病患者的预后。然而,仍然缺乏令人信服的证据证明它们在银屑病的发病机制中的重要性,生物体能否引发银屑病的发展仍有待确定。

  5、 银屑病抵御真菌感染

  银屑病是一种全身炎症性疾病,其中免疫系统的失调导致炎性因子的表达增高,而这些炎症因子参与宿主防御的常见感染。Th17在银屑病患者的体内表达增高,主要通过上调中性粒细胞趋化因子如CXCL1和CXCL5,抗微生物肽如人β-防御素(HBD)和其他促炎细胞因子抗感染(Conti & Gaffen 2015)。角质形成细胞在IL-17的刺激下产生CXCL1和CXCL3,作用于中性粒细胞,促进其向表皮迁移,促进局部组织破坏及影响角质形成细胞的分化(Nograles et al. 2008)。与抗IL-17治疗的银屑病患者临床观察到的CXCL1表达降低和中性粒细胞几乎完全清除相关(Reich et al. 2015)。

  人类抗菌肽的主要成分为Cathelicidins(LL-37)、β-防御素2(hBD-2)以及S100蛋白。糠秕马拉色菌通过蛋白激酶C处理48h后上调了hBD-2,TGFβ-1和IL-10的表达,证明了防御素在抵御马拉色菌入侵的重要作用(Donnarumma et al. 2004)。Baroni et al.(2006)用糠秕马拉色菌感染角质形成细胞后,发现TLR2、MyD88、hBD-2、hBD-3和IL-8mRNA上调,并且在银屑病患者皮肤活检中也证实了这一现象,说明通过产生hBD-2和角质形成细胞来源的趋化因子(例如IL-8)的释放募集中心粒细胞到感染部位消灭病原体。LL-37是人类cathelicidin家族中唯一的成员,Tsai et al.(2014)研究了LL-37对白色念珠菌细胞壁和细胞应答的影响,证明LL-37在白念珠菌中诱导复杂的反应起到抗真菌的作用,并且有研究指出cathelicidin可以用来预防口腔白色念珠菌感染,尤其是涉及生物膜的慢性感染(Yu et al. 2016)。Hein et al.(2015)发现银屑病患者的psoriasin(S100A7)以其二硫化物还原形式(redS100A7)作为人体表面的主要抗真菌因子。redS100A7抑制丝状真菌及曲霉的生长,主要通过穿透真菌细胞膜并通过新形成的基于硫基的金属结合位点从细胞内靶区中分离Zn2+来诱导真菌细胞凋亡。

  IL-17和Th17细胞在真菌免疫中具有重要的保护作用,特别是对共生的白色念珠菌(Huppler et al. 2012;Ling & Puel 2014),因此银屑病患者高表达的IL-17可以一定程度上抑制白念珠菌等真菌的感染。但是抗IL-17治疗后并没有导致慢性皮肤黏膜念珠菌病或系统性念珠菌病。并且在停止抗IL-17治疗后,试验证明小鼠自发清除了体内的白色念珠菌感染。由此可知,阻断体内IL-17A以短暂,轻度至中度以及可逆的方式抑制了其对白色念珠菌的保护性免疫作用(Whibley et al. 2016)。因此,IL-17或许只有一定程度上抑制真菌感染的作用,并不能作为抵御真菌感染的主要途径。

  6、 结论

  综上所述,各种实验室研究以及临床研究都证实了真菌感染与银屑病相互影响。研究真菌与银屑病之间的关系,可以决定未来是否将抗真菌治疗加入到银屑病的辅助治疗当中。研究者可从抗真菌治疗对于银屑病的影响探讨两者之间的关系,也可从免疫学角度进一步研究真菌诱发或加重银屑病皮损的具体机制,从而提高银屑病的治疗效果以及改善患者的预后。

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作者单位:中山大学孙逸仙纪念医院皮肤性病科
原文出处:蓝雨,席丽艳,张军民.皮肤真菌感染与银屑病的相关性[J/OL].菌物学报:1-7[2019-07-19].https://doi.org/10.13346/j.mycosystema.190089.
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