Effect of rpoS mutations on stress-resistance and invasion of brain microvascular endothelial cells in Escherichia coli K1

Ying Wang, Kwang Sik Kim

Research output: Contribution to journalArticlepeer-review

Abstract

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. Copyright (C) 2000 Federation of European Microbiological Societies.

Original languageEnglish (US)
Pages (from-to)241-247
Number of pages7
JournalFEMS microbiology letters
Volume182
Issue number2
DOIs
StatePublished - Jan 15 2000

Keywords

  • Brain microvascular endothelial cell invasion
  • Escherichia coli K1
  • Growth medium
  • Nonsense mutation
  • RpoS
  • Sigma factor

ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology
  • Genetics

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