Alteration of immunoproteome profile of Echinococcus granulosus hydatid fluid with progression of cystic echinococcosis.
Alteration of immunoproteome profile of Echinococcus granulosus hydatid fluid with progression of cystic echinococcosis.
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随着囊性棘球菌病的进展，甲状腺棘球菌的免疫蛋白质组谱的变化。
DOI：
10.1186/s13071-014-0610-7
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发表时间：
2015-01-08
影响因子：
3.2
通讯作者：
Kong Y
中科院分区：
文献类型：
--
作者：
Ahn CS;Han X;Bae YA;Ma X;Kim JT;Cai H;Yang HJ;Kang I;Wang H;Kong Y
囊型包虫病是由细粒棘球绦虫后鞭虫引起的一种严重的公共卫生问题。早期诊断对减少伤残调整寿命年有很大影响。已知有几个抗原B相关分子(EgAgB；EgAgB1-5)具有免疫潜力，但在许多患者中，EgAgB的检测是不同的，可能不能可靠地解释其免疫学相关性。更重要的是，包虫体液(HF)的免疫蛋白质组图谱尚未得到解决。我们用双向电泳法(2-DE)对CE1和CE2期单个可育包囊的HF进行了蛋白质组学分析。用基质辅助激光解吸电离飞行时间质谱仪(MALDI-TOF-MS)分析每个蛋白质斑点。随后，我们使用了从CE1到CE5阶段的整个疾病谱的患者血清，确定了免疫蛋白质组图谱。我们鉴定了40种寄生虫蛋白，其中EgAgB(28个点)和抗原5(EgAg5；5个分子)含量丰富。EgAgB蛋白形式占多数，主要是EgAgB1(24个点)，其次是EgAgB2和EgAgB4(各2个点)。只能用高效液相色谱-MS/MS检测到EgAgB3，不能识别EgAgB5。我们还检测到38种宿主蛋白，它们主要由血清成分、抗氧化剂/异源酶和与碳水化合物代谢有关的酶组成。CE1和CE2HF具有相似的斑点模式，但CE2HF含有更多的EgAgB和EgAg5复合体。CE2和CE3阶段对不同的EgAgB和EgAg5蛋白有较强的抗体反应，而CE1、CE4和CE5阶段主要与EgAg5和组织蛋白酶B反应。泡型包虫病患者血清与不同的EgAgB亚型发生交叉反应(36%)。EgAg5和组织蛋白酶B也与脑囊虫病和裂头蚴病血清发生交叉反应。我们的结果表明，检测单个确定的分子可能不能正确诊断CE，因为特定的免疫优势表位随着疾病的进展而改变。免疫蛋白质组分析结合影像研究在CE与AE和其他囊性病变的鉴别诊断以及CE的分期方面可能是实用的，这对于建立适当的患者管理是有意义的。本文的在线版本(doi：10.1186/s13071-0140610-7)包含补充材料，授权用户可以使用。
Cystic echinococcosis (CE), caused by Echinococcus granulosus metacestode, invokes a serious public health concern. Early diagnosis has great impacts on reduction of disability-adjusted life years. Several antigen B-related molecules (EgAgB; EgAgB1-5) are known to be immunopotent, but detection of EgAgB is variable in many patients and may not allow reliable interpretation of its immunological relevance. More importantly, the immunoproteome profile of hydatid fluid (HF) has not been addressed. We conducted a proteome analysis of the HF of a single fertile cyst of CE1 and CE2 stages through two-dimensional electrophoresis (2-DE). Each protein spot was analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). We subsequently determined the immunoproteome profile employing patient sera of entire disease spectrum from CE1 to CE5 stages. We identified 40 parasite proteins, of which EgAgB (28 spots) and antigen 5 (EgAg5; 5 molecules) were abundant. EgAgB proteoforms constituted the majority, mostly EgAgB1 (24 spots), followed by EgAgB2 and EgAgB4 (2 spots each). EgAgB3 was detected only by liquid chromatography-MS/MS. EgAgB5 was not recognized. We also detected 38 host proteins, which were largely composed of serum components, antioxidant/xenobiotic enzymes, and enzymes involved in carbohydrate metabolism. CE1 and CE2 HF exhibited comparable spotting patterns, but CE2 HF harbored greater amounts of EgAgB and EgAg5 complexes. CE sera demonstrated complicated immune recognition patterns according to the disease progression; CE2 and CE3 stages exhibited strong antibody responses against diverse EgAgB and EgAg5 proteoforms, while CE1, CE4, and CE5 stages mainly reacted to EgAg5 and cathepsin B. Patient sera of alveolar echinococcosis (AE) cross-reacted with diverse EgAgB isoforms (36%). EgAg5 and cathepsin B also demonstrated cross-reactions with sera from neurocysticercosis and sparganosis. Our results demonstrated that detection of a single defined molecule may not properly diagnose CE, since specific immunodominant epitopes changed as the disease progresses. Immunoproteome analysis combined with imaging studies may be practical in the differential diagnosis of CE from AE and other cystic lesions, as well as for staging CE, which are pertinent to establish appropriate patient management. The online version of this article (doi:10.1186/s13071-014-0610-7) contains supplementary material, which is available to authorized users.
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