Dynamics of connective-tissue localization during chronic Borrelia burgdorferi infection

The etiologic agent of Lyme disease, Borrelia burgdorferi, localizes preferentially in the extracellular matrix during persistence. In chronically infected laboratory mice, there is a direct association between B. burgdorferi and the proteoglycan decorin, which suggests that decorin has a role in de...

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Bibliographic Details
Published in:Laboratory investigation 2013-08, Vol.93 (8), p.900-910
Main Authors: Imai, Denise M, Feng, Sunlian, Hodzic, Emir, Barthold, Stephen W
Format: Article
Language:English
Subjects:
Animals
Borrelia burgdorferi
Borrelia burgdorferi - isolation & purification
Borrelia burgdorferi - physiology
Cellular Microenvironment
Collagen Type I - metabolism
Connective Tissue - metabolism
Connective Tissue - microbiology
Connective Tissue - pathology
decorin
Decorin - metabolism
decorin-binding proteins
Disease Models, Animal
Female
Host-Pathogen Interactions
Immunization, Passive
Immunocompromised Host
Lyme disease
Lyme Disease - metabolism
Lyme Disease - microbiology
Lyme Disease - pathology
Mice
Mice, Inbred C3H
Mice, SCID
mouse model
Spirochaetales - physiology
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Summary:The etiologic agent of Lyme disease, Borrelia burgdorferi, localizes preferentially in the extracellular matrix during persistence. In chronically infected laboratory mice, there is a direct association between B. burgdorferi and the proteoglycan decorin, which suggests that decorin has a role in defining protective niches for persistent spirochetes. In this study, the tissue colocalization of B. burgdorferi with decorin and the dynamics of borrelial decorin tropism were evaluated during chronic infection. Spirochetes were found to colocalize absolutely with decorin, but not collagen I in chronically infected immunocompetent C3H mice. Passive immunization of infected C3H-scid mice with B. burgdorferi-specific immune serum resulted in the localization of spirochetes in decorin-rich microenvironments, with clearance of spirochetes from decorin-poor microenvironments. In passively immunized C3H-scid mice, tissue spirochete burdens were initially reduced, but increased over time as the B. burgdorferi-specific antibody levels waned. Concurrent repopulation of the previously cleared decorin-poor microenvironments was observed with the rising tissue spirochete burden and declining antibody titer. These findings indicate that the specificity of B. burgdorferi tissue localization during chronic infection is determined by decorin, driven by the borrelia-specific antibody response, and fluctuates with the antibody response.
ISSN:0023-6837
1530-0307
DOI:10.1038/labinvest.2013.81