Calvinho L F, Oliver S P
Department of Animal Science, University of Tennessee, Knoxville 37901-1071, USA.
J Dairy Sci. 1998 Mar;81(3):678-86. doi: 10.3168/jds.S0022-0302(98)75623-1.
Little is known about bacterial and host factors that contribute to the establishment and persistence of intramammary infection by Streptococcus dysgalactiae. Streptococcus dysgalactiae adheres to epithelial cells from the bovine mammary gland and to extracellular matrix proteins in vitro and invades mammary epithelial cell cultures, all of which can be potentially important pathogenic mechanisms. In this study, mechanisms involved in the invasion of Strep. dysgalactiae into epithelial cells from the bovine mammary gland were characterized. Studies were conducted to determine whether Strep. dysgalactiae invaded mammary epithelial cell cultures in a dose-dependent manner and whether mammary epithelial cells that harbored different numbers of Strep. dysgalactiae for varying times were damaged. Bacterial invasion increased as inoculum size increased; however, the number of intracellular bacteria was not proportional to the inoculum size, increased; however, the number of intracellular bacteria was not proportional to the inoculum size, indicating that a finite number of organisms is capable of invading epithelial cells. No net increase in intracellular organisms was detected at any bacterial density evaluated; however, Strep. dysgalactiae remained viable throughout the evaluation. In addition, Strep. dysgalactiae did not appear to cause cell injury at any bacterial density or time point evaluated. These data suggest that Strep. dysgalactiae can survive within mammary epithelial cells for an extended time without losing viability or damaging the eukaryotic cell. This feature may be associated with the development of persistent infection and protection of organisms from antimicrobial drugs and host defense mechanisms and may provide a route for bacterial colonization of subepithelial tissues.
关于促成乳房链球菌引起乳腺内感染的建立和持续存在的细菌及宿主因素,人们所知甚少。乳房链球菌在体外可黏附于牛乳腺上皮细胞及细胞外基质蛋白,并侵入乳腺上皮细胞培养物,所有这些都可能是潜在的重要致病机制。在本研究中,对乳房链球菌侵入牛乳腺上皮细胞的机制进行了表征。开展研究以确定乳房链球菌是否以剂量依赖性方式侵入乳腺上皮细胞培养物,以及在不同时间携带不同数量乳房链球菌的乳腺上皮细胞是否受损。随着接种量增加,细菌侵袭增加;然而,细胞内细菌数量与接种量不成正比,这表明有限数量的微生物能够侵入上皮细胞。在评估的任何细菌密度下均未检测到细胞内微生物的净增加;然而,在整个评估过程中乳房链球菌均保持存活。此外,在评估的任何细菌密度或时间点,乳房链球菌似乎均未造成细胞损伤。这些数据表明,乳房链球菌可在乳腺上皮细胞内长时间存活,而不会丧失活力或损伤真核细胞。这一特性可能与持续性感染的发展以及微生物对抗菌药物和宿主防御机制的保护有关,并可能为细菌在皮下组织的定植提供一条途径。