Wang Y, Kim K S
Division of Infectious Diseases, MS #51, Childrens Hospital Los Angeles, the University of Southern California School of Medicine, Los Angeles, CA 90027, USA.
FEMS Microbiol Lett. 2000 Jan 15;182(2):241-7. doi: 10.1111/j.1574-6968.2000.tb08902.x.
Escherichia coli K1 strains are predominant in causing neonatal meningitis. We have shown that invasion of brain microvascular endothelial cells (BMEC) is a prerequisite for E. coli K1 crossing of the blood-brain barrier. BMEC invasion by E. coli K1 strain RS218, however, has been shown to be significantly greater with stationary-phase cultures than with exponential-phase cultures. Since RpoS participates in regulating stationary-phase gene expression, the present study examined a possible involvement of RpoS in E. coli K1 invasion of BMEC. We found that the cerebrospinal fluid isolates of E. coli K1 strains RS218 and IHE3034 have a nonsense mutation in their rpoS gene. Complementation with the E. coli K12 rpoS gene significantly increased the BMEC invasion of E. coli K1 strain IHE3034, but failed to significantly increase the invasion of another E. coli K1 strain RS218. Of interest, the recovery of E. coli K1 strains following environmental insults was 10-100-fold greater on Columbia blood agar than on LB agar, indicating that growing medium is important for viability of rpoS mutants after environmental insults. Taken together, our data suggest that the growth-phase-dependent E. coli K1 invasion of BMEC is affected by RpoS and other growth-phase-dependent regulatory mechanisms.
大肠杆菌K1菌株是引起新生儿脑膜炎的主要病菌。我们已经表明，侵袭脑微血管内皮细胞（BMEC）是大肠杆菌K1穿越血脑屏障的先决条件。然而，研究表明，与对数期培养物相比，大肠杆菌K1菌株RS218在稳定期培养物中对BMEC的侵袭能力明显更强。由于RpoS参与调节稳定期基因表达，因此本研究检测了RpoS在大肠杆菌K1侵袭BMEC过程中可能发挥的作用。我们发现，大肠杆菌K1菌株RS218和IHE3034的脑脊液分离株在其rpoS基因中存在无义突变。用大肠杆菌K12的rpoS基因进行互补可显著增强大肠杆菌K1菌株IHE3034对BMEC的侵袭能力，但未能显著增强另一株大肠杆菌K1菌株RS218的侵袭能力。有趣的是，在受到环境损伤后，大肠杆菌K1菌株在哥伦比亚血琼脂上的复苏能力比在LB琼脂上高10到100倍，这表明生长培养基对rpoS突变体在环境损伤后的生存能力很重要。综上所述，我们的数据表明，大肠杆菌K1对BMEC的生长阶段依赖性侵袭受到RpoS和其他生长阶段依赖性调节机制的影响。
