Saturday, October 26, 2013

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

This study is pretty interesting and a bit unsettling, but I guess the findings are not exactly news, if you consider the reasons for a Herxheimer reaction while/after taking abx to 'kill the bugs.' It's known that neurotoxins can be created as the critters die off, which is why many LLMDs prefer a slow approach particularly in patients who have detox pathway challenges. Another reason we should all tank up on our antioxidants and nutrients that support the liver and kidneys.  -Bob

2013 Oct 21. pii: S0304-3940(13)00936-1. doi: 10.1016/j.neulet.2013.10.032. [Epub ahead of print]

Parthasarathy G, Fevrier HB, Philipp MT.

Source

Division of Bacteriology and Parasitology, Tulane National Primate Research Center, 18703, Three Rivers Road, Covington, LA-7043,USA.

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.

Copyright © 2013. Published by Elsevier Ireland Ltd.

To see the article abstract and related links:

http://www.ncbi.nlm.nih.gov/pubmed/?term=Non-viable+Borrelia+burgdorferi+induce

1 comment:

  1. Having not seen the complete paper, I would be wondering if they put any time span on this:

    " 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."

    Left over for how long? Continue to be pathogenic for how long? Why would normal processes of removing damaged cells and other debris not make this a short term effect? And it seems like this still does not say anything about relapsing and the response to antibiotics when resumed in symptomatic patients with some treatment already. Why would antibiotic treatment do anything about dead spirochetes, without assuming magical anti-inflammatory properties for all antibiotics? If this explained continuing symptoms in all cases, then non-antibiotic anti-inflammatories like aspirin, etc. ought to be working just as well, but they don't.

    In the absence of more information, this just seems to muddy the water. If the letter does not answer these questions, they need to do it because as a broad statement to explain "post lyme syndrome," this does not.

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