Lyme neuroborreliosis is a nervous system
infectious disease caused by Borrelia burgdorferi (B. burgdorferi). It has been demonstrated that
cytokines induced by B. burgdorferi are related to
Lyme neuroborreliosis. Microglia is known as a key player in the immune responses that occur within the central nervous system. In response to
inflammation, it will be activated and generate
cytokines and
chemokines. Experiments in vitro cells have showed that B. Burgdorferi
membrane protein A (BmpA), a major immunogen of B. Burgdorferi, could induce
Lyme arthritis and stimulate human and murine lymphocytes to produce inflammatory
cytokines. In our study, the murine microglia BV2 cell line was used as a cell model to explore the stimulating effects of recombinant BmpA (rBmpA);
Chemokine chip, ELISA and QPCR technology were used to measure the production of
chemokines from microglial cells stimulated by rBmpA. Compared with the negative control group, CXCL2, CCL22, and CCL5 concentrations in the cell supernatant increased significantly after the rBmpA stimulation; the concentration of these
chemokines increased with rBmpA concentration increasing; the
mRNA expression levels of
chemokines (CXCL2, CCL22, and CCL5) in murine BV2 cells increased significantly with 10 μg/mL and 20 μg/mL rBmpA stimulation; CXCL13 was not change after the rBmpA stimulation. Our study shows that
chemokines, such as CXCL2, CCL22, and CCL5 were up-regulated by the rBmpA in the BV2 cells. The production of
chemokines in
Lyme neuroborreliosis may be mainly from microglia cells and the rBmpA may be closely related with the development of
Lyme neuroborreliosis.