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Background  Lyme disease is a common vector-borne disease caused by the spirochete  Borrelia burgdorferi  ( Bb ), which manifests as systemic and targeted tissue inflammation. Both  in vitro  and  in vivo  studies have shown that  Bb -induced inflammation is primarily host-mediated, via cytokine or chemokine production that promotes leukocyte adhesion/migration. Whether  Bb  produces mediators that can directly alter the vascular permeability  in vivo  has not been investigated. The objective of the present study was to investigate if  Bb  produces a mediator(s) that can directly activate endothelial cells resulting in increases in permeability in intact microvessels in the absence of blood cells.    Methodology/Principal Findings  The effects of cell-free, spent culture medium from virulent (B31-A3) and avirulent (B31-A)  B. burgdorferi  on microvessel permeability and endothelial calcium concentration, [Ca 2+ ] i , were examined in individually perfused rat mesenteric venules. Microvessel permeability was determined by measuring hydraulic conductivity (Lp). Endothelial [Ca 2+ ] i , a necessary signal initiating hyperpermeability, was measured in Fura-2 loaded microvessels. B31-A3 spent medium caused a rapid and transient increase in Lp and endothelial [Ca 2+ ] i . Within 2–5 min, the mean peak Lp increased to 5.6±0.9 times the control, and endothelial [Ca 2+ ] i  increased from 113±11 nM to a mean peak value of 324±35 nM. In contrast, neither endothelial [Ca 2+ ] i  nor Lp was altered by B31-A spent medium.    Conclusions/Significance  A mediator(s) produced by virulent  Bb  under culture conditions directly activates endothelial cells, resulting in increases in microvessel permeability. Most importantly, the production of this mediator is associated with  Bb  virulence and is likely produced by one or more of the 8 plasmid(s) missing from strain B31-A.

Spent Culture Medium from Virulent Borrelia burgdorferi Increases Permeability of Individually Perfused Microvessels of Rat Mesentery