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炭疽芽孢杆菌毒素缺陷菌株诱导的保护性免疫

Protective immunity induced by Bacillus anthracis toxin-deficient strains.

作者信息

Pezard C, Weber M, Sirard J C, Berche P, Mock M

机构信息

Laboratoire de Génétique Moléculaire des Toxines (URA 1858, Centre National de la Recherche Scientifique), Institut Pasteur, Paris, France.

出版信息

Infect Immun. 1995 Apr;63(4):1369-72. doi: 10.1128/iai.63.4.1369-1372.1995.

DOI:10.1128/iai.63.4.1369-1372.1995
PMID:7890396
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC173160/
Abstract

The two toxins secreted by Bacillus anthracis are composed of binary combinations of three proteins: protective antigen (PA), lethal factor (LF), and edema factor (EF). Six mutant strains that are deficient in the production of one or two of these toxin components have been previously constructed and characterized (C. Pezard, E. Duflot, and M. Mock, J. Gen. Microbiol. 139:2459-2463, 1993). In this work, we examined the antibody response to the in vivo production of PA, LF, and EF in mice immunized with spores of strains producing these proteins. High titers of antibody to PA were observed after immunization with all strains producing PA, while titers of antibodies to EF and LF were weak in animals immunized with strains producing only EF or LF. In contrast, immunization with strains producing either PA and EF or PA and LF resulted in an increased antibody response to EF or LF, respectively. The differing levels of protection from a lethal anthrax challenge afforded to mice immunized with spores of the mutant strains not only confirm the role of PA as the major protective antigen in the humoral response but also indicate a significant contribution of LF and EF to immunoprotection. We observed, however, that PA-deficient strains were also able to provide some protection, thereby suggesting that immune mechanisms other than the humoral response may be involved in immunity to anthrax. Finally, a control strain lacking the toxin-encoding plasmid was unable to provide protection or elicit an antibody response against bacterial antigens, indicating a possible role for pXO1 in the survival of B. anthracis in a host.

摘要

炭疽芽孢杆菌分泌的两种毒素由三种蛋白质的二元组合构成

保护性抗原(PA)、致死因子(LF)和水肿因子(EF)。先前已构建并鉴定了六种在产生一种或两种这些毒素成分方面存在缺陷的突变菌株(C. Pezard、E. Duflot和M. Mock,《普通微生物学杂志》139:2459 - 2463,1993年)。在这项研究中,我们检测了用产生这些蛋白质的菌株的孢子免疫的小鼠体内对PA、LF和EF产生的抗体反应。在用所有产生PA的菌株免疫后,观察到针对PA的高滴度抗体,而在用仅产生EF或LF的菌株免疫的动物中,针对EF和LF的抗体滴度较弱。相反,用产生PA和EF或PA和LF的菌株免疫分别导致对EF或LF的抗体反应增强。用突变菌株的孢子免疫的小鼠在抵抗致死性炭疽攻击时所获得的不同程度的保护,不仅证实了PA作为体液反应中主要保护性抗原的作用,还表明LF和EF对免疫保护有重要贡献。然而,我们观察到缺乏PA的菌株也能够提供一定程度的保护,从而表明除体液反应之外的免疫机制可能参与了对炭疽的免疫。最后,一个缺乏毒素编码质粒的对照菌株无法提供保护或引发针对细菌抗原的抗体反应,这表明pXO1在炭疽芽孢杆菌在宿主体内的存活中可能发挥作用。

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