Lyme disease is the most common vector-borne disease in the United States and is typically caused by the bacterium Borrelia burgdorferi. Although often curable, delayed diagnosis due to nonspecific symptoms risks systemic complications, and some patients experience symptoms despite bacterial clearance from the body. We hypothesized that B. burgdorferi infection induces a self-perpetuating cascade of immunological responses such that symptoms remain after infection or causes residual damage to patients’ immune system and tissues. We present a transcriptome study of B. burgdorferi infection in murine heart and brain tissues using the Next Generation Sequencing technology and computational methods to identify differentially expressed genes, particularly for evidence of active inflammatory pathways. Our results reveal differential expression of five genes in an infected heart. These differentially expressed genes are enriched in pathways related to immune functions in heart tissue. Our study indicated that B. burgdorferi infection triggers immune response pathways similar to other pathogens, and some genes were found to be unique to infection by B. burdorferi, suggesting the potential for development of specific therapeutic targets to treat B. burgdorferi infection. In the brain, 66 genes were differentially expressed. These genes were enriched in pathways that facilitate the pathogen’s crossing of the blood-brain barrier. Although the mouse model of B. burgdorferi infection fails to recapitulate human neuroborreliosis, we observed damage to the integrity of the blood-brain barrier upon peripheral infection. This study elucidates mechanism of infection unique to Borrelia and clarifies the role of a mouse model of Lyme disease.
Title
A transcriptome study of Borrelia burgdorferi infection in murine heart and brain tissues
Carey, M. A. and E. S. Ho (2017 June) "A transcriptome study of Borrelia burgdorferi infection in murine heart and brain tissues." Journal of Young Investigators 33 (1): 28-41.