Decorin binding proteins A and B (
DbpA and B) of Borrelia burgdorferi are of critical importance for the virulence of the spirochete. The objective of the present study was to further clarify the contribution of
DbpA and B to development of
arthritis and persistence of B. burgdorferi after
antibiotic treatment in a murine model of
Lyme borreliosis. With that goal, mice were infected with B. burgdorferi strains expressing either
DbpA or DbpB, or both
DbpA and B, or with a strain lacking the adhesins.
Arthritis development was monitored up to 15 weeks after
infection, and bacterial persistence was studied after
ceftriaxone and immunosuppressive treatments. Mice infected with the B. burgdorferi strain expressing both
DbpA and B developed an early and prominent joint swelling. In contrast, while strains that expressed
DbpA or B alone, or the strain that was
DbpA and B deficient, were able to colonize mouse joints, they caused only negligible joint manifestations.
Ceftriaxone treatment at two or six weeks of
infection totally abolished joint swelling, and all
ceftriaxone treated mice were B. burgdorferi culture negative.
Antibiotic treated mice, which were immunosuppressed by anti-
TNF-alpha, remained culture negative. Importantly, among
ceftriaxone treated mice, B. burgdorferi
DNA was detected by PCR uniformly in joint samples of mice infected with
DbpA and B expressing bacteria, while this was not observed in mice infected with the
DbpA and B deficient strain. In conclusion, these results show that both
DbpA and B adhesins are crucial for early and prominent
arthritis development in mice. Also, post-treatment borrelial
DNA persistence appears to be dependent on the expression of
DbpA and B on B. burgdorferi surface. Results of the immunosuppression studies suggest that the persisting material in the joints of
antibiotic treated mice is
DNA or
DNA containing remnants rather than live bacteria.