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感染复数对单核细胞增生李斯特菌针对HeLa和Caco-2细胞系致病性的影响。

Effect of multiplicity of infection on Listeria monocytogenes pathogenicity for HeLa and Caco-2 cell lines.

作者信息

Francis M S, Thomas C J

机构信息

Department of Microbiology and Immunology, University of Adelaide, South Australia.

出版信息

J Med Microbiol. 1996 Nov;45(5):323-30. doi: 10.1099/00222615-45-5-323.

DOI:10.1099/00222615-45-5-323
PMID:8918946
Abstract

The significance of multiplicity of infection (moi) for invasiveness and intracellular multiplication of Listeria monocytogenes in Caco-2 and HeLa cell monolayers was investigated. A low moi (1:1) resulted in recovery of significantly more L. monocytogenes when these bacteria were used to infect either cell line. At high moi (100:1), the percentage recovery of bacteria was comparatively low, even after extensive invasion and intracellular multiplication. Microscopic analysis of Giemsa- and immunofluorescent-stained infected monolayers revealed extensive cell disruption and exposure of the internalised bacteria to the bactericidal effect of gentamicin. By contrast, a low moi resulted in minimal cytopathic effects and evidence of cell to cell spread by L. monocytogenes was consistently observed in HeLa and J774, but not in Caco-2 cell lines. Nevertheless, the use of HeLa and Caco-2 cell monolayers enabled a clear distinction to be made between invasive (L. monocytogenes) and non-invasive Listeria spp. (L. innocua, L. ivanovii, L. seeligeri, L. grayi, L. welshimeri and L. monocytogenes LLO19). The use of a low moi with HeLa cell monolayers provided a reliable tissue-culture model of infection for L. monocytogenes.

摘要

研究了感染复数(moi)对单核细胞增生李斯特菌在Caco-2和HeLa细胞单层中的侵袭性和细胞内增殖的意义。当用这些细菌感染任一细胞系时,低感染复数(1:1)导致回收的单核细胞增生李斯特菌显著更多。在高感染复数(100:1)时,即使经过广泛的侵袭和细胞内增殖,细菌的回收率相对较低。对吉姆萨染色和免疫荧光染色的感染单层进行显微镜分析,发现细胞广泛破坏,内化细菌暴露于庆大霉素的杀菌作用下。相比之下,低感染复数导致最小的细胞病变效应,并且在HeLa和J774细胞系中始终观察到单核细胞增生李斯特菌细胞间传播的证据,但在Caco-2细胞系中未观察到。然而,使用HeLa和Caco-2细胞单层能够明确区分侵袭性(单核细胞增生李斯特菌)和非侵袭性李斯特菌属(无害李斯特菌、伊氏李斯特菌、斯氏李斯特菌、格氏李斯特菌、威氏李斯特菌和单核细胞增生李斯特菌LLO19)。使用低感染复数和HeLa细胞单层为单核细胞增生李斯特菌提供了可靠的组织培养感染模型。

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