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Research Article Free access | 10.1172/JCI2325

A new animal model for studying Lyme disease spirochetes in a mammalian host-adapted state.

D R Akins, K W Bourell, M J Caimano, M V Norgard, and J D Radolf

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235, USA.

Find articles by Akins, D. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235, USA.

Find articles by Bourell, K. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235, USA.

Find articles by Caimano, M. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235, USA.

Find articles by Norgard, M. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235, USA.

Find articles by Radolf, J. in: JCI | PubMed | Google Scholar

Published May 15, 1998 - More info

Published in Volume 101, Issue 10 on May 15, 1998
J Clin Invest. 1998;101(10):2240–2250. https://doi.org/10.1172/JCI2325.
© 1998 The American Society for Clinical Investigation
Published May 15, 1998 - Version history
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Abstract

There is now substantial evidence that Borrelia burgdorferi, the Lyme disease spirochete, undergoes major alterations in antigenic composition as it cycles between its arthropod and mammalian hosts. In this report, we cultivated B. burgdorferi 297 within dialysis membrane chambers implanted into the peritoneal cavities of rats to induce antigenic changes similar to those which occur during mammalian infection. Chamber-grown spirochetes, which remained fully virulent, did not express either outer surface protein A or Lp6.6, lipoproteins known to be downregulated after mammalian infection. However, they did, express p21, a well characterized outer surface protein E homologue, which is selectively expressed during infection. SDS-PAGE, two-dimensional gel electrophoresis, and immunoblot analysis revealed that chamber-grown borreliae also expressed uncharacterized proteins not expressed by in vitro-cultivated spirochetes; reactivity with sera from mice chronically infected with B. burgdorferi 297 confirmed that many of these novel proteins are selectively expressed during experimental murine infection. Finally, we used differential display RT-PCR to identify transcripts of other differentially expressed B. burgdorferi genes. One gene (2.9-7lpB) identified with this technique belongs to a family of genes located on homologous 32- and 18-kb circular plasmids. The lipoprotein encoded by 2.9-7lpB was shown to be selectively expressed by chamber-grown spirochetes and by spirochetes during experimental infection. Cultivation of B. burgdorferi in rat peritoneal implants represents a novel system for studying Lyme disease spirochetes in a mammalian host-adapted state.

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