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从炭疽芽孢杆菌细胞表面释放的低分子胶囊对炭疽发病机制的影响。

Effect of the lower molecular capsule released from the cell surface of Bacillus anthracis on the pathogenesis of anthrax.

作者信息

Makino Sou-Ichi, Watarai Masahisa, Cheun Hyeng-Il, Shirahata Toshikazu, Uchida Ikuo

机构信息

Department of Veterinary Microbiology, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Hokkaido 080-8555, Japan.

出版信息

J Infect Dis. 2002 Jul 15;186(2):227-33. doi: 10.1086/341299. Epub 2002 Jun 27.

DOI:10.1086/341299
PMID:12134259
Abstract

Bacillus anthracis enters the body as an endospore, and encapsulation and toxin production occur after germination. Capsule is proposed to be an antiphagocytic factor, and toxin induces cytokine production for systemic shock. The dep gene, adjacent to the cap region for the encapsulation, degrades the high-molecular weight capsule (H-capsule) to the lower-molecular weight capsule (L-capsule), which releases into the culture supernatant. This study analyzed the biological function of the cap-dep region. The dep null mutant Sm-1, which formed H-capsule but not L-capsule, was avirulent. However, Sm-1 with an intact dep gene or with purified L-capsule recovered its pathogenicity. Sm-1 was subjected to phagocytosis by macrophages more easily than its parent strain, Sm, in vitro; in vivo, it cleared without L-capsule and grew well with L-capsule, which suggests that L-capsule is essential for in vivo multiplication. Moreover, a new name, capD, might be appropriate, because of the part of the cap operon involved in both polymerization and depolymerization of the capsule.

摘要

炭疽芽孢杆菌以芽孢形式进入机体,发芽后发生荚膜形成和毒素产生。荚膜被认为是一种抗吞噬因子,毒素可诱导细胞因子产生导致全身休克。dep基因与荚膜形成的cap区域相邻,可将高分子量荚膜(H-荚膜)降解为低分子量荚膜(L-荚膜),后者释放到培养上清中。本研究分析了cap-dep区域的生物学功能。缺失dep的突变体Sm-1形成H-荚膜但不形成L-荚膜,无致病性。然而,具有完整dep基因的Sm-1或添加纯化L-荚膜后恢复了致病性。体外实验中,Sm-1比其亲本菌株Sm更容易被巨噬细胞吞噬;在体内,没有L-荚膜时Sm-1被清除,有L-荚膜时生长良好,这表明L-荚膜对于体内增殖至关重要。此外,由于cap操纵子中参与荚膜聚合和解聚的部分,一个新名称capD可能是合适的。

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