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缺乏磷脂酰肌醇特异性磷脂酶C的单核细胞增生李斯特菌突变体无致病性。

Listeria monocytogenes mutants lacking phosphatidylinositol-specific phospholipase C are avirulent.

作者信息

Camilli A, Goldfine H, Portnoy D A

机构信息

Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia 19104.

出版信息

J Exp Med. 1991 Mar 1;173(3):751-4. doi: 10.1084/jem.173.3.751.

DOI:10.1084/jem.173.3.751
PMID:1847723
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2118838/
Abstract

A number of bacterial species secrete phosphatidylinositol-specific phospholipase C (PI-PLC). In this report, we show that the facultative intracellular bacterial pathogen, Listeria monocytogenes, contains a gene, plcA, predicting a polypeptide with 31% amino acid identity to a Bacillus thuringiensis PI-PLC. Accordingly, L. monocytogenes secretes PI-PLC activity, while a mutant with a transposon insertion in plcA lacks detectable PI-PLC activity. In addition, expression of plcA in B. subtilis resulted in secretion of PI-PLC activity. The L. monocytogenes PI-PLC-defective mutant was three logs less virulent for mice and failed to grow in host tissues. The mutant was also defective for in vitro growth in mouse peritoneal macrophages. These results strongly suggest that PI-PLC is an essential determinant of L. monocytogenes pathogenesis. Whether the PI-PLC acts on a bacterial or host substrate remains to be determined.

摘要

许多细菌物种会分泌磷脂酰肌醇特异性磷脂酶C(PI-PLC)。在本报告中,我们表明兼性胞内细菌病原体单核细胞增生李斯特菌含有一个基因plcA,预测其编码的多肽与苏云金芽孢杆菌PI-PLC有31%的氨基酸同一性。相应地,单核细胞增生李斯特菌分泌PI-PLC活性,而在plcA中插入转座子的突变体缺乏可检测到的PI-PLC活性。此外,plcA在枯草芽孢杆菌中的表达导致PI-PLC活性的分泌。单核细胞增生李斯特菌PI-PLC缺陷型突变体对小鼠的毒力降低了三个对数级,并且无法在宿主组织中生长。该突变体在小鼠腹腔巨噬细胞中的体外生长也存在缺陷。这些结果强烈表明PI-PLC是单核细胞增生李斯特菌致病机制的一个关键决定因素。PI-PLC作用于细菌还是宿主底物仍有待确定。

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Listeria monocytogenes mutants lacking phosphatidylinositol-specific phospholipase C are avirulent.缺乏磷脂酰肌醇特异性磷脂酶C的单核细胞增生李斯特菌突变体无致病性。
J Exp Med. 1991 Mar 1;173(3):751-4. doi: 10.1084/jem.173.3.751.
2
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