In a new study from Tulane University, researchers found remnants of B. burgdorferi, the bacteria that causes Lyme disease, may contribute to inflammation in both the central and peripheral nervous systems.
Previous studies have shown that some Lyme disease patients suffer from an array of symptoms including neurological issues that greatly diminish their quality of life, even after the antibiotic treatment.
Brain scans of these patients show persistent neuroinflammation, but the cause has been unclear.
In the current study, the team examined the effects of B. burgdorferi remnants on nervous system tissue using a nonhuman primate model, investigating the effects on both the frontal cortex and dorsal root ganglion.
They found that inflammatory markers in these areas were several times higher in samples exposed to remnants of B. burgdorferi than in samples exposed to live bacteria, and several times higher in the frontal cortex than the dorsal root ganglion.
The bacterial remnants also caused cell death in brain neurons.
The findings suggest that antibiotics may kill the bacteria in human organs, but remnants could remain if the body cannot adequately eliminate them. The unresolved bacterial fragments could cause long-term health consequences.
Scientists still don’t know how B. burgdorferi spirochetes find their way into brain tissue.
They are planning future studies to investigate new anti-inflammatory therapies for antibiotic-resistant neuroinflammation and to explore why the body may not be clearing these bacterial remnants.
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The study was conducted by Geetha Parthasarathy et al. and published in Scientific Reports.
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