In previous studies, exposure to live Borrelia burgdorferi was shown to induce inflammation and apoptosis of human oligodendrocytes. In this study we assessed the ability of non-viable bacteria (heat killed or sonicated) to induce inflammatory mediators and cell death. Both heat-killed and sonicated bacteria induced release of CCL2, IL-6, and CXCL8 from oligodendrocytes in a dose dependent manner. In addition, non-viable B. burgdorferi also induced cell death as evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and another cell viability assay. These results suggest that spirochetal residues left after bacterial demise, due to treatment or otherwise, may continue to be pathogenic to the central nervous system.
Keywords: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Apoptosis; B. burgdorferi; ELISA; Inflammation; LB; Lyme borreliosis; Lyme neuroborreliosis; MTT; Oligodendrocytes; PMA; PTLDS; TUNEL; enzyme-linked immuno sorbent assay; phorbol myristate acetate; post-treatment Lyme disease syndrome; terminal deoxynucleotidyl transferase dUTP nick end labeling.
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