Altered murine tissue colonization by Borrelia burgdorferi following targeted deletion of linear plasmid 17-carried genes

Timothy Casselli; Yvonne Tourand; Troy Bankhead

doi:10.1128/IAI.05984-11

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Altered murine tissue colonization by Borrelia burgdorferi following targeted deletion of linear plasmid 17-carried genes

Journal article

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Peer reviewed

Altered murine tissue colonization by Borrelia burgdorferi following targeted deletion of linear plasmid 17-carried genes

Timothy Casselli, Yvonne Tourand and Troy Bankhead

Infection and immunity, Vol.80(5), pp.1773-1782

05/2012

DOI: https://doi.org/10.1128/IAI.05984-11

Handle:

https://hdl.handle.net/2376/104427

PMCID: PMC3347435

PMID: 22354033

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Abstract

Bacterial Proteins - genetics

Borrelia burgdorferi - physiology

Joints - microbiology

Mice, SCID

Genetic Complementation Test

Gene Expression Regulation, Bacterial - physiology

Mice, Inbred C3H

Animals

Borrelia burgdorferi - genetics

Ear - microbiology

Gene Deletion

Plasmids - genetics

Bacterial Proteins - metabolism

Mice

Urinary Bladder - microbiology

Heart - microbiology

Immunocompromised Host

Lyme Disease - microbiology

The causative agent of Lyme disease, Borrelia burgdorferi, possesses a segmented genome comprised of a single linear chromosome and upwards of 23 linear and circular plasmids. Much of what is known about plasmid-borne genes comes from studying laboratory clones that have spontaneously lost one or more plasmids during in vitro passage. Some plasmids, including the linear plasmid lp17, are never or rarely reported to be lost during routine culture; therefore, little is known about the requirement of these conserved plasmids for infectivity. In this study, the effects of deleting regions of lp17 were examined both in vitro and in vivo. A mutant strain lacking the genes bbd16 to bbd25 showed no deficiency in the ability to establish infection or disseminate to the bloodstream of mice; however, colonization of peripheral tissues was delayed. Despite the ability to colonize ear, heart, and joint tissues, this mutant exhibited a defect in bladder tissue colonization for up to 56 days postinfection. This phenotype was not observed in immunodeficient mice, suggesting that bladder colonization by the mutant strain was inhibited by an adaptive immune-based mechanism. Moreover, the mutant displayed increased expression of outer surface protein C in vitro, which was correlated with the absence of the gene bbd18. To our knowledge, this is the first report involving genetic manipulation of lp17 in an infectious clone of B. burgdorferi and reveals for the first time the effects of lp17 gene deletion during murine infection by the Lyme disease spirochete.

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Title: Altered murine tissue colonization by Borrelia burgdorferi following targeted deletion of linear plasmid 17-carried genes
Creators: Timothy Casselli - Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington, USA
Yvonne Tourand
Troy Bankhead
Publication Details: Infection and immunity, Vol.80(5), pp.1773-1782
Academic Unit: Veterinary Microbiology and Pathology, Department of
Publisher: United States
Identifiers: 99900546728401842
Language: English
Resource Type: Journal article