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血吸虫性肉芽肿调节。III. 埃及血吸虫加速曼氏血吸虫可溶性虫卵抗原在体内诱导的肝肉芽肿形成。

Schistosomal granuloma modulation. III. Schistosma haematobium worms accelerate S. mansoni soluble egg antigen-induced hepatic granuloma formation in vivo.

作者信息

Jacobs W, Deelder A, Bogers J, Van de Vijver K, Van Marck E

机构信息

Department of Pathology, University of Antwerp (UIA), Belgium.

出版信息

Parasitol Res. 1999 Nov;85(11):905-9. doi: 10.1007/s004360050656.

DOI:10.1007/s004360050656
PMID:10540951
Abstract

Recurrent experimental evidence indicates that schistosomal egg granuloma formation at least in the murine model results from a host response generated against both egg- and worm-derived antigens. Further experiments aimed at identifying the existence in vivo of cross-sensitization between Schistosoma haematobium worms and S. mansoni-derived egg antigens were performed with respect to S. mansoni egg antigen-induced granuloma formation and fibrogenesis in the liver. Male OF1 mice bisexually infected with S. haematobium or S. mansoni were hepatically challenged (cecal vein injection) with S. mansoni SEA (soluble egg antigen)-coupled Sepharose beads at the end of prepatent infection (8-10 days prior to the start of egg deposition). The mean granuloma volume (MGV) of in-vivo-generated synchronized hepatic granulomas (8 days old) and the fibrotic response were estimated. Just like S. mansoni-infected rodents, mice carrying an S. haematobium infection generated an accelerated hepatic granulomogenesis [respective MGVs 4.72 +/- 0.56 and 5.41 +/- 0.75 x 10(6) microm3; P < 0.0001 versus unsensitized (MGV 3.00 +/- 0.40 x 10(6) microm3) mice] and an enhanced fibrotic response against S. mansoni SEA. They also had significantly enlarged spleens (P < 0.0001) and moderately enlarged livers (P = 0.02) as compared with S. haematobium-infected mice that were not challenged with SEA. From these observations we infer that in vivo, S. haematobium worms can positively modulate S. mansoni egg antigen-induced granuloma formation and hepatic fibrogenesis, resulting in more severe liver pathology.

摘要

反复的实验证据表明,至少在鼠模型中,血吸虫卵肉芽肿的形成是宿主针对虫卵和虫体来源抗原产生的反应所致。针对埃及血吸虫虫体与曼氏血吸虫来源的虫卵抗原之间体内交叉致敏的存在情况,开展了进一步实验,研究对象为曼氏血吸虫虫卵抗原诱导的肝脏肉芽肿形成和纤维化。在潜伏期感染末期(虫卵沉积开始前8 - 10天),用与曼氏血吸虫可溶性虫卵抗原(SEA)偶联的琼脂糖珠经盲肠静脉注射对双性感染埃及血吸虫或曼氏血吸虫的雄性OF1小鼠进行肝脏攻击。对体内生成的同步化肝脏肉芽肿(8日龄)的平均肉芽肿体积(MGV)和纤维化反应进行了评估。与感染曼氏血吸虫的啮齿动物一样,感染埃及血吸虫的小鼠产生了加速的肝脏肉芽肿形成[各自的MGV分别为4.72±0.56和5.41±0.75×10(6)立方微米;与未致敏(MGV为3.00±0.40×10(6)立方微米)小鼠相比,P<0.0001]以及针对曼氏血吸虫SEA的增强纤维化反应。与未用SEA攻击的感染埃及血吸虫的小鼠相比,它们的脾脏也明显肿大(P<0.0001),肝脏中度肿大(P = 0.02)。从这些观察结果我们推断,在体内,埃及血吸虫虫体能正向调节曼氏血吸虫虫卵抗原诱导的肉芽肿形成和肝脏纤维化,导致更严重的肝脏病变。

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