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ColV质粒和K1抗原对大肠杆菌致病性的相对贡献

Relative contribution of ColV plasmid and K1 antigen to the pathogenicity of Escherichia coli.

作者信息

Agüero M E, Cabello F C

出版信息

Infect Immun. 1983 Apr;40(1):359-68. doi: 10.1128/iai.40.1.359-368.1983.

Abstract

To study the relevance of the ColV plasmid and the capsular K1 antigen in the pathogenicity of Escherichia coli, isogenic strains that differ only in these characteristics were constructed. Studies with these variants demonstrated that the presence of the ColV plasmid increased the serum resistance of E. coli. This increase did not depend on the expression of the K1 antigen. This work also demonstrated that the presence of the K1 antigen protects E. coli from the bactericidal activity of serum. Studies using mouse peritoneal macrophages in the presence of normal serum indicated that the presence of K1 antigen protects E. coli from phagocytosis. Similar experiments with the K1(+) strains performed in the presence of anti-K1 antibodies demonstrated that these antibodies opsonized these bacteria very efficiently in the absence of complement. The K1(-)E. coli variants were efficiently phagocytized in the presence of normal human serum and absorbed human serum, indicating that they are able to be opsonized by complement deposited by activation of the alternative pathway of complement. Work using fluorescence microscopy confirmed that the K1(-) strains are able to fix complement in the absence of antibody. It was also found that the presence of the ColV plasmid may interfere with phagocytosis of the E. coli K1 strains and deposition of complement on these cells. To test the relevance of the results of the in vitro experiments for disease, the pathogenicity of the strains was tested in mice. The results showed that the K1 antigen is the main determinant of pathogenicity of these strains and that the presence of ColV can modify the pathogenic potential of the E. coli K1 strains through a mechanism that does not depend on the production of colicin V.

摘要

为研究ColV质粒和荚膜K1抗原在大肠杆菌致病性中的相关性,构建了仅在这些特征上存在差异的同基因菌株。对这些变体的研究表明,ColV质粒的存在增加了大肠杆菌的血清抗性。这种增加不依赖于K1抗原的表达。这项工作还表明,K1抗原的存在可保护大肠杆菌免受血清的杀菌活性影响。在正常血清存在下使用小鼠腹腔巨噬细胞进行的研究表明,K1抗原的存在可保护大肠杆菌免受吞噬作用。在抗K1抗体存在下对K1(+)菌株进行的类似实验表明,在没有补体的情况下,这些抗体能非常有效地调理这些细菌。K1(-)大肠杆菌变体在正常人血清和吸收性人血清存在下能被有效吞噬,表明它们能够被通过补体替代途径激活而沉积的补体调理。使用荧光显微镜的研究证实,K1(-)菌株在没有抗体的情况下能够固定补体。还发现ColV质粒的存在可能会干扰大肠杆菌K1菌株的吞噬作用以及补体在这些细胞上的沉积。为了测试体外实验结果与疾病的相关性,在小鼠中测试了这些菌株的致病性。结果表明,K1抗原是这些菌株致病性的主要决定因素,并且ColV的存在可通过一种不依赖于产大肠杆菌素V的机制改变大肠杆菌K1菌株的致病潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b81/264856/a05d0fde52e7/iai00139-0373-a.jpg

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