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Infection and Immunity, October 2006, p. 5609-5616, Vol. 74, No. 10
0019-9567/06/$08.00+0     doi:10.1128/IAI.00321-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Effects of ompA Deletion on Expression of Type 1 Fimbriae in Escherichia coli K1 Strain RS218 and on the Association of E. coli with Human Brain Microvascular Endothelial Cells

Ching-Hao Teng,2,3 Yi Xie,1 Sooan Shin,1 Francescopaolo Di Cello,1 Maneesh Paul-Satyaseela,1 Mian Cai,1 and Kwang Sik Kim1*

Division of Pediatric Infectious Diseases, School of Medicine, Johns Hopkins University, Baltimore, Maryland 21287,1 Division of Clinical Research, National Health Research Institutes, Tainan, Taiwan,2 Institute of Molecular Medicine, National Cheng Kung University Medical College, Tainan, Taiwan3

Received 27 February 2006/ Returned for modification 31 May 2006/ Accepted 20 July 2006

We have previously shown that outer membrane protein A (OmpA) and type 1 fimbriae are the bacterial determinants involved in Escherichia coli K1 binding to human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier. In investigating the role of OmpA in E. coli K1 binding to HBMEC, we showed for the first time that ompA deletion decreased the expression of type 1 fimbriae in E. coli K1. Decreased expression of type 1 fimbriae in the ompA deletion mutant was largely the result of driving the fim promoter toward the type 1 fimbrial phase-OFF orientation. mRNA levels of fimB and fimE were found to be decreased with the OmpA mutant compared to the parent strain. Of interest, the ompA deletion further decreased the abilities of E. coli K1 to bind to and invade HBMEC under the conditions of fixing type 1 fimbria expression in the phase-ON or phase-OFF status. These findings suggest that the decreased ability of the OmpA mutant to interact with HBMEC is not entirely due to its decreased type 1 fimbrial expression and that OmpA and type 1 fimbriae facilitate the interaction of E. coli K1 with HBMEC at least in an additive manner.

* 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{at}jhmi.edu.

Editor: F. C. Fang

Infection and Immunity, October 2006, p. 5609-5616, Vol. 74, No. 10
0019-9567/06/$08.00+0     doi:10.1128/IAI.00321-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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