Distinct characteristics of resistance to Borrelia burgdorferi-induced arthritis in C57BL/6N mice.
Studies of mice infected with Borrelia burgdorferi have indicated that the severity of arthritis is influenced by the genetic composition of the host: the C3H mouse develops severe arthritis while BALB/c and C57BL/6 mice develop mild arthritis. In this study, the effects of increasing infectious dose on the severity of arthritis were determined in these three mouse strains. C3H/He mice developed severe arthritis at all infectious doses, with 100% infection requiring 200 spirochetes. In BALB/cAnN mice, arthritis severity was dependent on infectious dose; symptoms were mild with infection by 200 B. burgdorferi and progressively more severe with increasing infectious dose. Infection of BALB/cAnN mice with 2 x 10(4) B. burgdorferi resulted in arthritis with severity identical to that in C3H/He mice. Spirochete levels in rear ankle joints of C3H/HeJ and C3H/HeN mice were relatively high, as detected by PCR, and did not increase with infectious dose. Spirochete levels in joints from BALB/cAnN mice increased with increasing infectious dose to levels found in severely arthritic C3H/He mice. Thus, resistance to severe arthritis in BALB/cAnN mice was conditional: it could be overcome by high infectious dose and the arthritis became severe when high levels of B. burgdorferi were present in joints. A unique response to increasing infectious dose was seen in C57BL/6N mice, which displayed mild to moderate arthritis at all doses of B. burgdorferi tested, up to 2 x 10(5). At all infectious doses, the levels of spirochetes in ankle joints of C57BL/6N mice were high, equivalent to those found in the severely arthritic C3H/He mice. The arthritis observed in infected (C57BL/6N x C3H/HeN)F1 mice was of severity intermediate between those of the two parental strains. The finding that resistance to severe arthritis in C57BL/6N mice could not be overcome by high infectious doses and was independent of spirochete levels in joints suggested that it was mediated by a distinct mechanism from that operating in BALB/cAnN mice.
Ma
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Department of Pathology, University of Utah School of Medicine, Salt Lake City 84132, USA.
Seiler
K P
KP
Eichwald
E J
EJ
Weis
J H
JH
Teuscher
C
C
Weis
J J
JJ
D000818:Animals; D000907:Antibodies, Bacterial / Q000032:analysis; D001170:Arthritis, Infectious / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D015748:Borrelia burgdorferi Group / Q000235:genetics / Q000302:isolation & purification; D015169:Colony Count, Microbial; D004269:DNA, Bacterial / Q000032:analysis / Q000235:genetics / Q000302:isolation & purification; D006790:Host-Parasite Interactions / Q000235:genetics; D007113:Immunity, Innate / Q000235:genetics*; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D008193:Lyme Disease / Q000235:genetics* / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D016133:Polymerase Chain Reaction; D013643:Tarsus, Animal / Q000382:microbiology / Q000473:pathology
D000907:Antibodies, Bacterial; D004269:DNA, Bacterial; D007074:Immunoglobulin G; D007075:Immunoglobulin M