| Literature DB >> 24157855 |
Geetha Parthasarathy1, Helene B Fevrier, Mario T Philipp.
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.Entities:
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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Year: 2013 PMID： 24157855 PMCID： PMC3856578 DOI： 10.1016/j.neulet.2013.10.032
Source DB: PubMed Journal: Neurosci Lett ISSN： 0304-3940 Impact factor: 3.046