NF-κB is a key modulator in the signaling pathway of Borrelia burgdorferi BmpA-induced inflammatory chemokines in murine microglia BV2 cells

Lyme disease, caused by the bacterial spirochete Borrelia burgdorferi, is a tick-borne zoonosis. Lyme neuroborreliosis is a principal manifestation of Lyme disease and its pathogenesis remains incompletely understood. Recent studies have demonstrated that Borrelia burgdorferi lipoproteins caused similar inflammatory effects as exhibited in Lyme neuroborreliosis. Basic membrane protein A (BmpA) is one of the dominant lipoproteins in the Borrelia burgdorferi membrane. In addition, nuclear factor κ-B (NF-κB) modulates the regulation of gene transcription associated with immunity and inflammation; however, in unstimulated cells, NF-κB is combined with the inhibitor of NF-κB (IκB-β). Therefore, it was hypothesized that NF-κB may be associated with BmpA-induced inflammation and the occurrence of Lyme neuroborreliosis. Therefore, the aim of the present study was to investigate the role that NF-κB serves in the signaling pathway of rBmpA-induced inflammatory chemokines. The present study measured the expression levels of NF-κB, IκB-β and inflammatory chemokines following recombinant BmpA (rBmpA) stimulation of murine microglia BV2 cells. Following stimulation with rBmpA, concentrations of pro-inflammatory cytokines including C-X-C motif chemokine 2, C-C motif chemokine (CCL) 5 and CCL22 were determined by ELISA analysis. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to detect the expression levels of NF-κB p65 and IκB-β. The data demonstrated that concentrations of these chemokines in cell supernatants increased significantly following rBmpA stimulation. NF-κB was overexpressed, but IκB-β expression was significantly decreased. In conclusion, these results suggested that NF-κB serves an important stimulatory role in the signaling pathway of rBmpA-induced inflammatory chemokines in BV2 cells.