AI Article Synopsis
- The study demonstrates that OmpA and type 1 fimbriae are key factors for E. coli K1's ability to bind to human brain microvascular endothelial cells, which form the blood-brain barrier.
- Deleting the ompA gene leads to reduced type 1 fimbriae expression and altered regulation of the fim promoter, contributing to a decrease in binding and invasion capabilities of E. coli K1.
- The findings indicate that while reduced fimbriae expression affects binding, OmpA also plays a significant role, suggesting a combined effect of both factors in facilitating the interaction with endothelial cells.
Article Abstract
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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1594875 | PMC |
| http://dx.doi.org/10.1128/IAI.00321-06 | DOI Listing |
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