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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.

DOI:10.1099/00222615-15-1-43
PMID:7143425
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。

相似文献

1
Role of bacterial adhesion in the pathogenesis of cholera.细菌黏附在霍乱发病机制中的作用。
J Med Microbiol. 1982 Feb;15(1):43-51. doi: 10.1099/00222615-15-1-43.
2
Role of somatic antigen of Vibrio cholerae in adhesion to intestinal mucosa.
J Med Microbiol. 1982 Feb;15(1):53-61. doi: 10.1099/00222615-15-1-53.
3
Neutralisation of the new cholera toxin by antiserum against crude enterotoxin of cholera toxin gene-positive Vibrio cholerae 01 in rabbit ileal loop model.在兔回肠袢模型中,霍乱毒素基因阳性霍乱弧菌01型粗肠毒素抗血清对新型霍乱毒素的中和作用。
Indian J Med Res. 1989 May;89:117-20.
4
Events in the pathogenesis of experimental cholera: role of bacterial adherence and multiplication.
J Med Microbiol. 1980 Feb;13(1):1-9. doi: 10.1099/00222615-13-1-1.
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Experimental studies on cholera immunization. 4. The antibody response to formalinized Vibrio cholerae and purified endotoxin with special reference to protective capacity.霍乱免疫的实验研究。4. 针对甲醛处理的霍乱弧菌和纯化内毒素的抗体反应,特别提及保护能力。
Int Arch Allergy Appl Immunol. 1975;49(4):434-52.
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Production of the new cholera toxin by environmental isolates of Vibrio cholerae non-O1.霍乱弧菌非O1群环境分离株产生新型霍乱毒素。
J Med Microbiol. 1996 Jul;45(1):31-4. doi: 10.1099/00222615-45-1-31.
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Specific antibodies to cholera toxin in rabbit milk are protective against Vibrio cholerae-induced intestinal secretion.兔奶中针对霍乱毒素的特异性抗体可预防霍乱弧菌引起的肠道分泌。
Immunology. 1987 Aug;61(4):543-7.
8
Vibrio cholerae cytolysin is essential for high enterotoxicity and apoptosis induction produced by a cholera toxin gene-negative V. cholerae non-O1, non-O139 strain.霍乱弧菌细胞毒素对于霍乱毒素基因阴性的霍乱弧菌非O1、非O139菌株产生的高肠毒性和诱导细胞凋亡至关重要。
Microb Pathog. 2008 Feb;44(2):118-28. doi: 10.1016/j.micpath.2007.08.013. Epub 2007 Aug 31.
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Role of exopolysaccharide, the rugose phenotype and VpsR in the pathogenesis of epidemic Vibrio cholerae.胞外多糖、粗糙型表型和VpsR在霍乱弧菌流行株致病机制中的作用
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RpoS controls the Vibrio cholerae mucosal escape response.RpoS控制霍乱弧菌的黏膜逃逸反应。
PLoS Pathog. 2006 Oct;2(10):e109. doi: 10.1371/journal.ppat.0020109.

引用本文的文献

1
Demonstration of lipopolysaccharide on sheathed flagella of Vibrio cholerae O:1 by protein A-gold immunoelectron microscopy.通过蛋白A-金免疫电子显微镜法证实霍乱弧菌O:1的鞘鞭毛上存在脂多糖
J Bacteriol. 1988 Apr;170(4):1488-94. doi: 10.1128/jb.170.4.1488-1494.1988.