The effects of Escherichia coli S-fimbriae and outer membrane protein A on rat pial arterioles

Cerebral vascular injury is common in bacterial meningitis, but the role of microbial factors associated with this phenomenon is unclear. Escherichia coli S-fimbriae and outer membrane protein A (OmpA) have been shown to promote binding and invasion of E. coli to brain microvascular endothelial cells, respectively. Using the cranial window model, we compared the response of pial arterioles in experimental animals exposed to E. coli with and without S-fimbriae or OmpA after intracarotid injection to animals receiving saline (control). After 3 h, pial arteriolar diameter had progressively increased to 144 ± 23 (SD)% of the baseline value in animals exposed to S-fimbriated E. coli and to 131 ± 12% of the baseline value in animals exposed to nonfimbriated E. coli. Analysis of variance with Bonferroni post hoc comparisons revealed that at 2 h the pial arteriolar response to S-fimbriated E. coli was significantly different from control (p = 0.0142). After 3 h, the S-fimbriated E. coli group was significantly different from both the control and the nonfimbriated group (p = 0.0024 and 0.0163, respectively). The nonfimbriated group showed a trend of progressive vasodilatation, which was not significantly different from the control. After 3 h, pial arteriolar diameter progressively increased to 156 ± 14% of baseline in animals exposed to OmpA⁺ E. coli and 151 ± 24% of baseline to OmpA - E. coli. The vasodilatory response to OmpA⁺ and OmpA^- E. coli was statistically different from control (p = 0.0004 and 0.0010, respectively) but not different from each other. These data suggest that, although cerebral vasodilatory response to E. coli is multifactorial, binding plays an important role in initiating the vasodilatation and bacterial invasion does not enhance the vasodilatory response in the cerebral microvasculature.