The early dissemination defect attributed to disruption of decorin-binding proteins is abolished in chronic murine lyme borreliosis

Denise Imai, D. Scott Samuels, Sunlian Feng, Emir Hodzic, Kim Olsen, Stephen W Barthold

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

The laboratory mouse model of Lyme disease has revealed that Borrelia burgdorferi differentially expresses numerous outer surface proteins that influence different stages of infection (tick-borne transmission, tissue colonization, dissemination, persistence, and tick acquisition). Deletion of two such outer surface proteins, decorin-binding proteins A and B (DbpA/B), has been documented to decrease infectivity, impede early dissemination, and, possibly, prevent persistence. In this study, DbpA/B-deficient spirochetes were confirmed to exhibit an early dissemination defect in immunocompetent, but not immunodeficient, mice, and the defect was found to resolve with chronicity. Development of disease (arthritis and carditis) was attenuated only in the early stage of infection with DbpA/B-deficient spirochetes in both types of mice. Persistence of the DbpA/B-deficient spirochetes occurred in both immunocompetent and immunodeficient mice in a manner indistinguishable from that of wild-type spirochetes. Dissemination through the lymphatic system was evaluated as an underlying mechanism for the early dissemination defect. At 12 h, 3 days, 7 days, and 14 days postinoculation, DbpA/B-deficient spirochetes were significantly less prevalent and in lower numbers in lymph nodes than wild-type spirochetes. However, in immunodeficient mice, deficiency of DbpA/B did not significantly decrease the prevalence or spirochete numbers in lymph nodes. Complementation of DbpA/B restored a wild-type phenotype. Thus, the results indicated that deficiency of DbpA/B allows the acquired immune response to restrict early dissemination of spirochetes, which appears to be at least partially mediated through the lymphatic system.

Original languageEnglish (US)
Pages (from-to)1663-1673
Number of pages11
JournalInfection and Immunity
Volume81
Issue number5
DOIs
StatePublished - May 2013

Fingerprint

Decorin
Spirochaetales
Lyme Disease
Staphylococcal Protein A
Carrier Proteins
Lymphatic System
Membrane Proteins
Lymph Nodes
Tick-Borne Diseases
Borrelia burgdorferi
IgA receptor
Myocarditis
Ticks
Protein Binding
Arthritis
Phenotype

ASJC Scopus subject areas

  • Immunology
  • Microbiology
  • Parasitology
  • Infectious Diseases

Cite this

The early dissemination defect attributed to disruption of decorin-binding proteins is abolished in chronic murine lyme borreliosis. / Imai, Denise; Scott Samuels, D.; Feng, Sunlian; Hodzic, Emir; Olsen, Kim; Barthold, Stephen W.

In: Infection and Immunity, Vol. 81, No. 5, 05.2013, p. 1663-1673.

Research output: Contribution to journalArticle

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