Abstract
This review describes the current knowledge of the pathogenesis of acute Lyme neuroborreliosis (LNB), from invasion to inflammation of the central nervous system. Borrelia burgdorferi (B.b.) enters the host through a tick bite on the skin and may disseminate from there to secondary organs, including the central nervous system. To achieve this, B.b. first has to evade the hostile immune system. In a second step, the borrelia have to reach the central nervous system and cross the blood-brain barrier. Once in the cerebrospinal fluid (CSF), the spirochetes elicit an inflammatory response. We describe current knowledge about the infiltration of leukocytes into the CSF in LNB. In the final section, we discuss the mechanisms by which the spirochetal infection leads to the observed neural dysfunction. To conclude, we construct a stringent concept of the pathogenesis of LNB.
Highlights
Lyme borreliosis is the most common human tick-borne disease in the Northern hemisphere
The complement system is a biochemical cascade that is potentially cytotoxic, and opsonizes the pathogen and attracts leukocytes [21]. The leukocytes constitute another threat for B.b.: different borrelial surface lipoproteins are recognized by leukocytes, mainly by CD14 and the toll-like receptor 2 (TLR2) of the innate immune system [17,22,23,24], and it has been shown in vitro that the spirochetes are rapidly taken up by polymorphonuclear cells, monocytes, and macrophages [25,26,27]
This hypothesis is further supported by the fact that a borrelial-induced chemokine, CXCL13, can be found in high concentrations in the cerebrospinal fluid (CSF), but not in the serum, of Lyme neuroborreliosis (LNB) patients in Europe
Summary
Lyme borreliosis is the most common human tick-borne disease in the Northern hemisphere. The complement system is a biochemical cascade that is potentially cytotoxic, and opsonizes the pathogen and attracts leukocytes [21] The leukocytes constitute another threat for B.b.: different borrelial surface lipoproteins are recognized by leukocytes, mainly by CD14 and the toll-like receptor 2 (TLR2) of the innate immune system [17,22,23,24], and it has been shown in vitro that the spirochetes are rapidly taken up by polymorphonuclear cells, monocytes, and macrophages [25,26,27]. Without the application of antibiotics, B.b. might persist in the mammalian host; chronic infections have been reported in the literature [5,30] Why is it so hard for the immune system to attack the borrelia?
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