• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文学位 >Immunological studies of the anti-inflammatory protein, Sj16, of Schistosoma japonicum.
【24h】

Immunological studies of the anti-inflammatory protein, Sj16, of Schistosoma japonicum.

机译：日本血吸虫抗炎蛋白Sj16的免疫学研究。

获取原文
获取原文并翻译 | 示例
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Schistosome is the causative agent of schistosomiasis which is one of the world's most prevalent tropical diseases. In the skin of infected host, significant inflammatory response to the parasite is not observed. Previous studies from Schistosoma mansoni showed that this subdued inflammatory response was due to a 16-KDa protein, Sm16, which is present abundantly in the secretions of schistosomulae. Provided that Schistosoma japonicum shares the same infective pathway as S. mansoni by penetrating the skin, it seems logical that S. japonicum has a protein with a similar role to Sm16 to down-regulate host immune responses. According to the cDNA sequence of Sm16, a corresponding gene (designated Sj16) of Sm16 has previously been amplified and cloned from the cercarial cDNA of S. japonicum. Sequence analysis showed that Sj16 shares 99% identity with Sm16 in its nucleotide sequence, and 100% identity in its protein sequence. While previous studiers reported their failure in obtaining the soluble recombinant protein of Sm16, we expressed and purified the recombinant Sj16 (rSj16) from E. coli in the present study. Western blot and ELISA analysis showed that S. japonicum-infected rabbit sera could not recognize rSj16, indicating that native Sj16 might fail to induce circulating antibodies during S. japonicum infection. In the in vivo study, rSj16 dramatically suppressed not only the recruitment of leukocytes to the peritoneal cavity of BALB/c mice injected with thioglycollate, but also the maturation of thioglycollate-induced peritoneal macrophages. The suppression effect was accompanied by a marked up-regulation of IL-10 and IL-1RA transcripts, and down-regulation of IL-12p35, IL-1beta and MIP-2 transcripts in peritoneal cells. Further analysis revealed that rSj16 also inhibited both humoral and cellular immune responses to heterologous antigens. In addition, rSj16 was found to induce macrophage differentiation of the murine myeloid leukemia WEHI-3B (JCS) cells, and regulate the differentiation of mouse hematopoietic cells towards the macrophage lineage. Although previous studies indicated the involvement of endogenous IL-1alpha, IL-1beta and TNF-alpha in the macrophage differentiation of JCS cells, the results from this study suggested that rSj16-induced JCS cell differentiation do not rely on the endogenous production of these three cytokines. This is the first study to successfully express and purify sufficient soluble rSj16, and demonstrate the anti-inflammatory and immunomodulatory effects of the rSj16.
机译：血吸虫是血吸虫病的病原体，血吸虫病是世界上最流行的热带病之一。在感染宿主的皮肤中，未观察到对寄生虫的明显炎症反应。曼氏血吸虫的先前研究表明，这种炎症反应减弱是由于16-KDa蛋白Sm16所致，该蛋白大量存在于血吸虫的分泌物中。如果日本血吸虫通过渗透皮肤与曼氏链球菌具有相同的感染途径，那么合乎逻辑的日本血吸虫具有与Sm16类似的蛋白，可以下调宿主的免疫反应。根据Sm16的cDNA序列，先前已经从日本血吸虫的子宫颈cDNA中扩增并克隆了Sm16的相应基因（称为Sj16）。序列分析表明，Sj16在其核苷酸序列中与Sm16具有99％的同一性，在其蛋白质序列中具有100％的同一性。尽管先前的研究人员报告了他们未能获得Sm16的可溶性重组蛋白，但在本研究中，我们从大肠杆菌表达并纯化了重组Sj16（rSj16）。 Western blot和ELISA分析表明，日本血吸虫感染的兔血清无法识别rSj16，表明天然Sj16在日本血吸虫感染期间可能无法诱导循环抗体。在体内研究中，rSj16不仅显着抑制了白细胞募集到注射巯基乙酸盐的BALB / c小鼠的腹腔中，而且还抑制了巯基乙酸盐诱导的腹膜巨噬细胞的成熟。抑制作用伴随着腹膜细胞中IL-10和IL-1RA转录物的明显上调，以及IL-12p35，IL-1beta和MIP-2转录物的下调。进一步的分析表明，rSj16还抑制了针对异源抗原的体液和细胞免疫反应。此外，发现rSj16可以诱导鼠骨髓性白血病WEHI-3B（JCS）细胞的巨噬细胞分化，并调节小鼠造血细胞向巨噬细胞谱系的分化。尽管先前的研究表明内源性IL-1α，IL-1β和TNF-α参与了JCS细胞的巨噬细胞分化，但这项研究的结果表明，rSj16诱导的JCS细胞分化并不依赖于这三种细胞的内源性产生。细胞因子。这是第一个成功表达和纯化足够的可溶性rSj16并证明rSj16的抗炎和免疫调节作用的研究。

著录项

  • 作者

    Hu, Shaomin.;

  • 作者单位

    The Chinese University of Hong Kong (Hong Kong).;

  • 授予单位 The Chinese University of Hong Kong (Hong Kong).;
  • 学科 Biology Parasitology.;Health Sciences Immunology.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 155 p.
  • 总页数 155
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号