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      Non-viable Borrelia burgdorferi induce inflammatory mediators and apoptosis in human oligodendrocytes.

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          Abstract

          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.

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          Author and article information

          Journal
          Neurosci. Lett.
          Neuroscience letters
          Elsevier BV
          1872-7972
          0304-3940
          Nov 27 2013
          : 556
          Affiliations
          [1 ] Division of Bacteriology and Parasitology, Tulane National Primate Research Center, 18703, Three Rivers Road, Covington LA-70433, USA.
          Article
          S0304-3940(13)00936-1 NIHMS534100
          10.1016/j.neulet.2013.10.032
          3856578

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