by Daniel J. Cameron, MD MPH
According to the authors, “If uncontrolled in the context of neuroborreliosis, the astrocyte response could lead to long-term injury in the CNS.”
Researchers identified changes in gene expression within 48 hours of infecting cultured astrocytes with Borrelia burgdorferi (Bb). “Understanding how these changes are maintained over time will be of great importance in developing effective treatments to Lyme disease,” according to Casselli and colleagues from the Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences. “If uncontrolled in the context of neuroborreliosis, the astrocyte response could lead to long-term injury in the CNS.” [1]
The study offers further insight into the role of Bb in neurocognitive changes in Lyme disease. “The pathophysiology behind the neurocognitive complaints of Lyme disease is unclear, but the inflammatory response to the bacterium or its components is likely to play a role,” according to Casselli. The authors also cited elevated serum IFN-α levels in patients with a history of Lyme disease and objective memory impairment [2] and apoptosis of neurons when human glia cells are stimulated with Bb. [3]
References:
- Casselli T, Qureshi H, Peterson E, Perley D, Blake E, Jokinen B, Abbas A, Nechaev S, Watt JA, Dhasarathy A et al: MicroRNA and mRNA Transcriptome Profiling in Primary Human Astrocytes Infected with Borrelia burgdorferi. PLoS One 2017, 12(1):e0170961.
- Jacek E, Fallon BA, Chandra A, Crow MK, Wormser GP, Alaedini A: Increased IFNalpha activity and differential antibody response in patients with a history of Lyme disease and persistent cognitive deficits. J Neuroimmunol 2012.
- Parthasarathy G, Fevrier HB, Philipp MT: Non-viable Borrelia burgdorferi induce inflammatory mediators and apoptosis in human oligodendrocytes. Neurosci Lett 2013, 556:200-203.
Leave a Reply