| Autor: |
Wang, Ying, Huang, Sheng-He, Wass, Carol A., Stins, Monique F., Kim, Kwang Sik |
| Zdroj: |
Infection and Immunity; September 1999, Vol. 67 Issue: 9 p4751-4756, 6p |
| Abstrakt: |
ABSTRACTMost cases of Escherichia colimeningitis develop as a result of hematogenous spread, but it is not clear how circulatingE. colicrosses the blood-brain barrier. A TnphoAmutant of E. coliK1 RS218 was shown to be significantly less invasive than its parent strain in bovine and human brain microvascular endothelial cells (BMEC), which constitute the blood-brain barrier. More importantly, traversal of the blood-brain barrier was significantly less with this mutant than with the parent strain in newborn rats with experimental hematogenous meningitis. A DNA segment containing the TnphoAinsertion site was cloned from RS218, and the cloned DNA complemented the TnphoAmutant in invasion of BMEC. Nucleotide sequence revealed a near identity to that of a hypothetical yijPgene (also calledf577) in the E. coliK-12 genome. Sequence analysis indicated that the E. coliK1 yijPgene likely encodes a 66.6-kDa membrane protein. Deletion and complementation experiments indicated that the yijPgene was involved in E. coliK1 invasion of BMEC, i.e., the invasive ability of E. coliK1 was significantly reduced after yijPwas deleted and was restored by complementation with a plasmid containing the yijPopen reading frame. This is the first demonstration that the yijPgene locus plays a role in the pathogenesis of E. coliK1 meningitis. |
| Databáze: |
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