Abstract
Borrelia burgdorferi, the agent of Lyme disease, has cholesterol and cholesterol-glycolipids that are essential for bacterial fitness, are antigenic, and could be important in mediating interactions with cells of the eukaryotic host. We show that the spirochetes can acquire cholesterol from plasma membranes of epithelial cells. In addition, through fluorescent and confocal microscopy combined with biochemical approaches, we demonstrated that B. burgdorferi labeled with the fluorescent cholesterol analog BODIPY-cholesterol or 3H-labeled cholesterol transfer both cholesterol and cholesterol-glycolipids to HeLa cells. The transfer occurs through two different mechanisms, by direct contact between the bacteria and eukaryotic cell and/or through release of outer membrane vesicles. Thus, two-way lipid exchange between spirochetes and host cells can occur. This lipid exchange could be an important process that contributes to the pathogenesis of Lyme disease.
Highlights
Borrelia burgdorferi, the causative agent of Lyme disease [1,2], is unusual among prokaryotes in that in addition to phosphatidylcholine, phosphatidylglycerol [3,4,5,6,7] and many different lipoproteins [4,5,8,9,10], it has free cholesterol and cholesterol-glycolipids in its outer membrane (OM)
Free cholesterol and cholesterol-glycolipids from B. burgdorferi are transferred to epithelial cells through direct contact and through outer membrane vesicles
We show here that there is a two-way exchange of lipids between B. burgdorferi and eukaryotic cells and that this exchange is accomplished through direct contact with the spirochete as well as contact with outer membrane vesicles (OMV)
Summary
The causative agent of Lyme disease [1,2], is unusual among prokaryotes in that in addition to phosphatidylcholine, phosphatidylglycerol [3,4,5,6,7] and many different lipoproteins [4,5,8,9,10], it has free cholesterol and cholesterol-glycolipids in its outer membrane (OM). Important to the pathogenesis of B. burgdorferi, ACGal, and to a lesser extent MGalD and CGal, are antigenic [13,15,16,17,19]. These glycolipids induce antibody responses throughout all stages of Lyme disease, being most prominent in the late stages [9,11,12,20,21]. Borrelia lipid antigens can be presented in the context of CD1d on NKT cells [24,25,26,27,28,29]
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