title: Borrelia burgdorferi RevA Significantly Affects Pathogenicity and Host Response in the Mouse Model of Lyme Disease.
abstract: The Lyme disease spirochete, Borrelia burgdorferi, expresses RevA and numerous outer surface lipoproteins during mammalian infection. As an adhesin that promotes bacterial interaction with fibronectin, RevA is poised to interact with the extracellular matrix of the host. To further define the role(s) of RevA during mammalian infection, we created a mutant that is unable to produce RevA. The mutant was still infectious to mice, although it was significantly less well able to infect cardiac tissues. Complementation of the mutant with a wild-type revA gene restored heart infectivity to wild-type levels. Additionally, revA mutants led to increased evidence of arthritis, with increased fibrotic collagen deposition in tibiotarsal joints. The mutants also induced increased levels of the chemokine CCL2, a monocyte chemoattractant, in serum, and this increase was abolished in the complemented strain. Therefore, while revA is not absolutely essential for infection, deletion of revA had distinct effects on dissemination, arthritis severity, and host response.
authors.affiliation: Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, USA.
authors.forename: Rebecca
authors.initials: R
authors.lastname: Byram
authors.affiliation: Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA.
authors.forename: Robert A
authors.initials: RA
authors.lastname: Gaultney
authors.affiliation: Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA.
authors.forename: Angela M
authors.initials: AM
authors.lastname: Floden
authors.affiliation: Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA.
authors.forename: Christopher
authors.initials: C
authors.lastname: Hellekson
authors.affiliation: Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA.
authors.forename: Brandee L
authors.initials: BL
authors.lastname: Stone
authors.affiliation: Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky School of Medicine, Lexington, Kentucky, USA.
authors.forename: Amy
authors.initials: A
authors.lastname: Bowman
authors.affiliation: Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky School of Medicine, Lexington, Kentucky, USA.
authors.forename: Brian
authors.initials: B
authors.lastname: Stevenson
authors.affiliation: Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, USA.
authors.forename: Barbara J B
authors.initials: BJ
authors.lastname: Johnson
authors.affiliation: Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA catherine.brissette@med.und.edu.
authors.forename: Catherine A
authors.initials: CA
authors.lastname: Brissette
mesh_terms: D000818:Animals; D001425:Bacterial Outer Membrane Proteins / Q000235:genetics* / Q000276:immunology; D015153:Blotting, Western; D025065:Borrelia burgdorferi / Q000472:pathogenicity*; D004195:Disease Models, Animal; D005260:Female; D055786:Gene Knockout Techniques; D008193:Lyme Disease / Q000235:genetics / Q000276:immunology* / Q000473:pathology*; D051379:Mice
chemical_list: D001425:Bacterial Outer Membrane Proteins; C434447:RevA protein, Borrelia burgdorferi