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The Lyme disease spirochete can hijack the host immune system for extravasation from the microvasculature
Author(s) -
Tan Xi,
Petri Björn,
DeVinney Rebekah,
Jenne Craig N.,
Chaconas George
Publication year - 2021
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.14728
Subject(s) - borrelia burgdorferi , biology , lyme disease , transcellular , extravasation , microbiology and biotechnology , paracellular transport , immune system , borrelia , immunology , antibody , genetics , membrane , permeability (electromagnetism)
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.