Escherichia coli K1 RS218 Interacts with Human Brain Microvascular Endothelial Cells via Type 1 Fimbria Bacteria in the Fimbriated State

Escherichia coli K1 is a major gram-negative organism causing neonatal meningitis. E. coli K1 binding to and invasion of human brain microvascular endothelial cells (HBMEC) are a prerequisite for E. coli penetration into the central nervous system in vivo. In the present study, we showed using DNA m...

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Published inInfection and Immunity Vol. 73; no. 5; pp. 2923 - 2931
Main Authors Teng, Ching-Hao, Cai, Mian, Shin, Sooan, Xie, Yi, Kim, Kee-Jun, Khan, Naveed Ahmed, Di Cello, Francescopaolo, Kim, Kwang Sik
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.05.2005
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Summary:Escherichia coli K1 is a major gram-negative organism causing neonatal meningitis. E. coli K1 binding to and invasion of human brain microvascular endothelial cells (HBMEC) are a prerequisite for E. coli penetration into the central nervous system in vivo. In the present study, we showed using DNA microarray analysis that E. coli K1 associated with HBMEC expressed significantly higher levels of the fim genes compared to nonassociated bacteria. We also showed that E. coli K1 binding to and invasion of HBMEC were significantly decreased with its fimH deletion mutant and type 1 fimbria locked-off mutant, while they were significantly increased with its type 1 fimbria locked-on mutant. E. coli K1 strains associated with HBMEC were predominantly type 1 fimbria phase-on (i.e., fimbriated) bacteria. Taken together, we showed for the first time that type 1 fimbriae play an important role in E. coli K1 binding to and invasion of HBMEC and that type 1 fimbria phase-on E. coli is the major population interacting with HBMEC.
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Editor: J. N. Weiser
Corresponding author. Mailing address: Division of Pediatric Infectious Diseases, School of Medicine, Johns Hopkins University, Baltimore, MD 21287. Phone: (410) 614-3917. Fax: (410) 614-1491. E-mail: kwangkim@jhmi.edu.
ISSN:0019-9567
1098-5522
DOI:10.1128/IAI.73.5.2923-2931.2005