Eric L. Brown, R. Mark Wooten, Barbara J.B. Johnson, Renato V. Iozzo, Amanda Smith, Marc C. Dolan, Betty P. Guo, Janis J. Weis, Magnus Höök
J Clin Invest. 2001;
107(7):845
doi:10.1172/JCI11692
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M
icrobial adhesion to the host tissue represents an early, critical step in the pathogenesis of most infectious diseases. Borrelia burgdorferi, the causative agent of Lyme disease (LD), expresses two surface-exposed decorin-binding adhesins, DbpA and DbpB. A decorin-deficient (Dcn–/–) mouse was recently developed and found to have a relatively mild phenotype. We have now examined the process of experimental LD in Dcn–/– mice using both needle inoculation and tick transmission of spirochetes. When exposed to low doses of the infective agent, Dcn–/– mice had fewer Borrelia-positive cultures from most tissues analyzed than did Dcn+/+ or Dcn+/– mice. When the infection dose was increased, similar differences were not observed in most tissues but were seen in bacterial colonization of joints and the extent of Borrelia-induced arthritis. Quantitative PCR demonstrated that joints harvested from Dcn–/– mice had diminished Borrelia numbers compared with issues harvested from Dcn+/+ controls. Histological examination also revealed a low incidence and severity of arthritis in Dcn–/– mice. Conversely, no differences in the numbers of Borrelia-positive skin cultures were observed among the different genotypes regardless of the infection dose. These differences, which were observed regardless of genetic background of the mice (BALB/c or C3H/HeN) or method of infection, demonstrate the importance of decorin in the pathogenesis of LD.