Kusters J G, Mulders-Kremers G A, van Doornik C E, van der Zeijst B A
Department of Bacteriology, Institute of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, University of Utrecht, The Netherlands.
Infect Immun. 1993 Dec;61(12):5013-20. doi: 10.1128/iai.61.12.5013-5020.1993.
Monolayers of intestine 407 (Int-407) cells were infected with the virulent Salmonella typhimurium strain C52, and the adhesion to and invasion of these cells were studied. The effects of the multiplicity of infection and growth phase of the bacteria (logarithmic versus stationary) on the interaction with eukaryotic cells were investigated. In contrast to other reports, we found no differences in the adhesive and invasive capacities of bacteria derived from logarithmic- or stationary-phase cultures. Invasion by S. typhimurium required bacterial protein synthesis and live Int-407 cells. Bacteria adhered equally well to dead or live Int-407 cells, which indicates that adhesion does not require metabolically active cells. Adhesion of S. typhimurium followed saturation kinetics, with a maximum of 10 adhesive bacteria per cell. This indicates that there is a limited number of bacterial adhesion sites (receptors) available on the surface of the host cell. Killed and live bacteria adhered equally well and competed with each other for cellular adhesion sites. This and adhesion experiments performed in the presence of chloramphenicol showed that bacterial protein synthesis is not required for adhesion. The general validity of the results obtained with S. typhimurium C52 was confirmed by comparing the invasion and adhesion data with those of the frequently used SL1344 and SR11 strains. In addition, we assayed the adhesion and invasion of S. typhimurium C52, SL1344, and SR11 and 27 S. typhimurium field isolates with Int-407, HeLa, and HEp-2 cells.
用强毒鼠伤寒沙门氏菌菌株C52感染单层肠407(Int-407)细胞,研究该菌对这些细胞的黏附与侵袭。研究了感染复数和细菌生长阶段(对数期与稳定期)对其与真核细胞相互作用的影响。与其他报道不同,我们发现对数期或稳定期培养物来源的细菌在黏附与侵袭能力上并无差异。鼠伤寒沙门氏菌的侵袭需要细菌蛋白质合成以及活的Int-407细胞。细菌对死的或活的Int-407细胞的黏附能力相同,这表明黏附并不需要代谢活跃的细胞。鼠伤寒沙门氏菌的黏附遵循饱和动力学,每个细胞最多有10个黏附细菌。这表明宿主细胞表面可用的细菌黏附位点(受体)数量有限。死菌和活菌的黏附能力相同,且相互竞争细胞黏附位点。这一点以及在氯霉素存在下进行的黏附实验表明,黏附不需要细菌蛋白质合成。通过将侵袭和黏附数据与常用的SL1344和SR11菌株的数据进行比较,证实了用鼠伤寒沙门氏菌C52获得的结果具有普遍有效性。此外,我们检测了鼠伤寒沙门氏菌C52、SL1344、SR11以及27株鼠伤寒沙门氏菌野外分离株对Int-407、HeLa和HEp-2细胞的黏附与侵袭情况。