Effect of rpoS mutations on stress-resistance and invasion of brain microvascular endothelial cells in Escherichia coli K1.
Effect of rpoS mutations on stress-resistance and invasion of brain microvascular endothelial cells in Escherichia coli K1.
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DOI：
10.1111/j.1574-6968.2000.tb08902.x
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发表时间：
2000
影响因子：
2.1
通讯作者：
Y. Wang;K. Kim
中科院分区：
文献类型：
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作者：
Y. Wang;K. Kim
大肠杆菌K1菌株是引起新生儿脑膜炎的主要菌株。我们已经证明，脑微血管内皮细胞（BMEC）的侵袭是E。coli K1通过血脑屏障。E.然而，稳定期培养物对大肠杆菌K1菌株RS 218的抑制作用显著高于指数期培养物。由于RpoS参与调节稳定期基因表达，本研究检测了RpoS在大肠杆菌中的可能参与。coli K1对BMEC的侵袭作用。我们发现脑脊液分离的E. coliK 1菌株RS 218和IHE 3034的rpoS基因存在无义突变。与E. coliK 12 rpoS基因可显著增强E. coli K1菌株IHE 3034的侵袭能力，但未能显著增加另一株E. coliK 1菌株RS 218。感兴趣的是，E. coli K1菌株在哥伦比亚血琼脂上的存活率比在LB琼脂上的高10-100倍，表明生长培养基对rpoS突变体在环境损伤后的存活率很重要。综上所述，我们的数据表明，生长阶段依赖的E。coli K1对BMEC的侵袭受到RpoS和其他生长期依赖性调控机制的影响。
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.