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Pathogen and Host Response Dynamics in a Mouse Model of Borrelia hermsii Relapsing Fever.
Crowder, Christopher D; Ghalyanchi Langeroudi, Arash; Shojaee Estabragh, Azadeh; Lewis, Eric R G; Marcsisin, Renee A; Barbour, Alan G.
Afiliación
  • Crowder CD; Departments of Microbiology & Molecular Genetics and Medicine, University of California Irvine, Irvine, CA 92697, USA. ccrowder@gmail.com.
  • Ghalyanchi Langeroudi A; Departments of Microbiology & Molecular Genetics and Medicine, University of California Irvine, Irvine, CA 92697, USA. arashghalyanchi@gmail.com.
  • Shojaee Estabragh A; Departments of Microbiology & Molecular Genetics and Medicine, University of California Irvine, Irvine, CA 92697, USA. ashojaiestabragh@gmail.com.
  • Lewis ERG; Departments of Microbiology & Molecular Genetics and Medicine, University of California Irvine, Irvine, CA 92697, USA. erlewis@utmb.edu.
  • Marcsisin RA; Departments of Microbiology & Molecular Genetics and Medicine, University of California Irvine, Irvine, CA 92697, USA. reneemarcsisin@gmail.com.
  • Barbour AG; Departments of Microbiology & Molecular Genetics and Medicine, University of California Irvine, Irvine, CA 92697, USA. abarbour@uci.edu.
Vet Sci ; 3(3)2016 Aug 30.
Article en En | MEDLINE | ID: mdl-29056727
Most Borrelia species that cause tick-borne relapsing fever utilize rodents as their natural reservoirs, and for decades laboratory-bred rodents have served as informative experimental models for the disease. However, while there has much progress in understanding the pathogenetic mechanisms, including antigenic variation, of the pathogen, the host side of the equation has been neglected. Using different approaches, we studied, in immunocompetent inbred mice, the dynamics of infection with and host responses to North American relapsing fever agent B. hermsii. The spirochete's generation time in blood of infected mice was between 4-5 h and, after a delay, was matched in rate by the increase of specific agglutinating antibodies in response to the infection. After initiating serotype cells were cleared by antibodies, the surviving spirochetes were a different serotype and, as a population, grew more slowly. The retardation was attributable to the host response and not an inherently slower growth rate. The innate responses at infection peak and immediate aftermath were characterized by elevations of both pro-inflammatory and anti-inflammatory cytokines and chemokines. Immunodeficient mice had higher spirochete burdens and severe anemia, which was accounted for by aggregation of erythrocytes by spirochetes and their partially reversible sequestration in greatly enlarged spleens and elsewhere.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Vet Sci Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Vet Sci Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza