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Updated: Nov 8, 2025
Methods for Rapid Transfer and Localization of Lyme Disease Pathogens Within the Tick Gut
Published on: February 14, 2011
The Lyme disease spirochete can hijack the host immune system for extravasation from the microvasculature
Xi Tan1, Björn Petri2, Rebekah DeVinney2
1Department of Biochemistry & Molecular Biology, Snyder Institute for Chronic Diseases, University of Calgary, Calgary, AB, Canada.
Abstract:
Lyme disease is the most common tick-transmitted disease in the northern hemisphere and is caused by the spirochete Borrelia burgdorferi and related Borrelia species. The constellation of symptoms attributable to this malady results from vascular dissemination of B. burgdorferi throughout the body to invade various tissue types. However, little is known about the mechanism by which the spirochetes can breach the blood vessel wall to reach distant tissues. We have studied this process by direct observation of spirochetes in the microvasculature of living mice using multi-laser spinning-disk intravital microscopy. Our results show that in our experimental system, instead of phagocytizing B. burgdorferi, host neutrophils are involved in the production of specific cytokines that activate the endothelium and potentiate B. burgdorferi escape into the surrounding tissue. Spirochete escape is not induced by paracellular permeability and appears to occur via a transcellular pathway. Neutrophil repurposing to promote bacterial extravasation represents a new and innovative pathogenic strategy.
Insights
Host neutrophils facilitate Borrelia burgdorferi (Lyme disease bacteria) spread by producing cytokines that help bacteria cross blood vessels. This neutrophil repurposing is a novel pathogenic strategy for bacterial dissemination.
Area of Science:
- Infectious Diseases
- Microbiology
- Immunology
Background:
- Lyme disease, caused by Borrelia burgdorferi, is a common tick-borne illness.
- B. burgdorferi disseminates through the bloodstream to infect various tissues.
- Mechanisms of Borrelia burgdorferi extravasation across the blood vessel wall remain unclear.
Purpose of the Study:
- To investigate the mechanism of Borrelia burgdorferi (B. burgdorferi) extravasation from the microvasculature.
- To elucidate the role of host immune cells in facilitating bacterial dissemination.
Main Methods:
- Utilized multi-laser spinning-disk intravital microscopy to observe B. burgdorferi in living mouse microvasculature.
- Analyzed host neutrophil interactions with B. burgdorferi and endothelial cells.
Main Results:
- Host neutrophils, rather than phagocytosing B. burgdorferi, produced cytokines that activated the endothelium.
- Endothelial activation potentiated B. burgdorferi escape into surrounding tissues via a transcellular pathway.
- B. burgdorferi extravasation was not mediated by increased paracellular permeability.
Conclusions:
- Neutrophil repurposing to promote bacterial extravasation is a novel pathogenic strategy employed by B. burgdorferi.
- Understanding this mechanism provides insights into Lyme disease pathogenesis and potential therapeutic targets.
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Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...