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细菌黏附在霍乱发病机制中的作用。

Role of bacterial adhesion in the pathogenesis of cholera.

作者信息

Chitnis D S, Sharma K D, Kamat R S

出版信息

J Med Microbiol. 1982 Feb;15(1):43-51. doi: 10.1099/00222615-15-1-43.

Abstract

In studies with the adult-rabbit ileal-loop model, antibodies to the lipopolysaccharide somatic-antigen component of Vibrio cholerae gave passive protection against challenge with live V. cholerae. The antisomatic antibodies had no effect on bacterial proliferation and toxin production either in vivo or in vitro; after challenge, antibody-protected and non-protected rabbit ileal loops developed almost identical amounts of cholera toxin and numbers of V. Cholerae. The protection could be correlated only with a 10-15-fold reduction in the number of V. cholerae adherent to the mucous membrane of the antibody-protected loops. The amount of cholera toxin in the two sets of loops ranged from 1600 to 3200 units. In contrast, when biologically active cholera toxin was prepared in vitro, the amount required to induce ileal-loop secretion was very large (25,600 units). These findings indicate that toxin production by adherent vibrios on the surface of the mucous membrane is an important factor in the pathogenesis of cholera.

摘要

在针对成年兔回肠袢模型的研究中,霍乱弧菌脂多糖菌体抗原成分的抗体对活霍乱弧菌攻击提供了被动保护。抗菌体抗体在体内或体外对细菌增殖及毒素产生均无作用;攻击后,抗体保护组和未保护组的兔回肠袢产生的霍乱毒素量及霍乱弧菌数量几乎相同。这种保护仅与抗体保护组回肠袢黏膜上霍乱弧菌附着数量减少10至15倍相关。两组回肠袢中的霍乱毒素量在1600至3200单位之间。相比之下,当在体外制备生物活性霍乱毒素时,诱导回肠袢分泌所需的量非常大(25,600单位)。这些发现表明,黏膜表面附着的弧菌产生毒素是霍乱发病机制中的一个重要因素。

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