Suppr超能文献

福氏志贺菌2a 34 kDa外膜蛋白在诱导保护性免疫反应中的作用

Role of Shigella flexneri 2a 34 kDa outer membrane protein in induction of protective immune response.

作者信息

Mukhopadhaya A, Mahalanabis D, Chakrabarti M K

机构信息

Division of Pathophysiology, National Institute of Cholera and Enteric Diseases, P-33, C.I.T. Road, Scheme-XM, Beliaghata, Kolkata 700010, West Bengal, India.

出版信息

Vaccine. 2006 Aug 14;24(33-34):6028-36. doi: 10.1016/j.vaccine.2006.03.026. Epub 2006 Mar 31.

Abstract

Emergence of Shigella vaccine is in great need in developing countries. In this paper we have shown that 34 kDa Shigella flexneri 2a outer membrane protein has a role in eliciting immune responses. When injected parentarally this protein gives significant protection against challenge with virulent Shigella flexneri 2a. Macrophages activated with the 34 kDa protein resulted in the dose dependent production of nitric oxide, the highly reactive free radical responsible for killing of invading bacterial pathogen. Also, treatment of murine peritoneal macrophages with the 34 kDa protein showed dose dependent increase in the production of tumor necrosis factor-alpha and interleukin-12. However, there was no dose dependent increase in interleukin-10 production. These data indicated that the 34 kDa outer membrane protein has the ability to modulate the protective immune response against the invading bacterial pathogen, mainly through TH1 mediated pathway. So, the 34 kDa outer mebrane protein can be one of the major components for developing subunit vaccine against shigellosis.

摘要

发展中国家迫切需要志贺氏菌疫苗。在本文中,我们已表明34 kDa福氏志贺氏菌2a外膜蛋白在引发免疫反应中发挥作用。当经肠胃外注射时,该蛋白能提供显著保护,抵御强毒性福氏志贺氏菌2a的攻击。用34 kDa蛋白激活的巨噬细胞会导致一氧化氮呈剂量依赖性产生,一氧化氮是负责杀死入侵细菌病原体的高活性自由基。此外,用34 kDa蛋白处理小鼠腹膜巨噬细胞显示肿瘤坏死因子-α和白细胞介素-12的产生呈剂量依赖性增加。然而,白细胞介素-10的产生没有剂量依赖性增加。这些数据表明,34 kDa外膜蛋白有能力调节针对入侵细菌病原体的保护性免疫反应,主要通过TH1介导的途径。因此,34 kDa外膜蛋白可以成为开发抗志贺氏菌病亚单位疫苗的主要成分之一。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验