| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
The evolution of Lyme borreliosis was examined in genetically resistant C.B.-17 and susceptible C3H/He(C3H) mice homozygous for the severe combined immune deficiency (scid) gene, or their immunocompetent counterparts. The C.B-17, C.B-17-scid, C3H, and C3H-scid mice were inoculated intradermally with 104 Borrelia burgdorferi and examined on days 14, 21, 30, 45, and 60 after inoculation. Spirochetemia was detected through 30 days, but was cleared in all groups by 45 days. Kidney and brain were inconsistently culture positive, but spleen and ear punch samples were positive in most mice. Immunocompetent C.B-17 and C3H mice seroconverted with equivalent IgG titers to B. burgdorferi, while C.B-17-scid and C3H-scid mice did not seroconvert. Arthritis occurred in nearly all joints examined in all genotypes on day 14, was of equal severity among C.B-17, C.B-17-scid, and C3H mice, but was more severe in C3H-scid mice. By days 30 and 45, arthritis began to resolve in immunocompetent mice, with C3H mice having more severe disease than C.B-17 mice. Arthritis persisted in C.B-17-scid and C3H-scid mice. Carditis occurred to an equal degree in all groups on day 14, remained active in scid mice, but regressed in immunocompetent mice at later intervals. Many spirochetes were visualized with silver stain in inflamed synovial tissues of scid mice, and were present in other tissues in smaller numbers. These studies show that specific immunity is not involved in arthritogenesis or genetically determined susceptibility to arthritis, but is involved in arthritis and carditis regression.
This article has been cited by other articles:
|
|
 |
|
  E. Hodzic, S. Feng, K. Holden, K. J. Freet, and S. W. Barthold Persistence of Borrelia burgdorferi following Antibiotic Treatment in Mice Antimicrob. Agents Chemother., May 1, 2008; 52(5): 1728 - 1736. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. P. Iliopoulou, J. Alroy, and B. T. Huber CD28 Deficiency Exacerbates Joint Inflammation upon Borrelia burgdorferi Infection, Resulting in the Development of Chronic Lyme Arthritis J. Immunol., December 15, 2007; 179(12): 8076 - 8082. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. O. Strother, E. Hodzic, S. W. Barthold, and A. M. de Silva Infection of Mice with Lyme Disease Spirochetes Constitutively Producing Outer Surface Proteins A and B Infect. Immun., June 1, 2007; 75(6): 2786 - 2794. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. J. Lazarus, M. J. Meadows, R. E. Lintner, and R. M. Wooten IL-10 Deficiency Promotes Increased Borrelia burgdorferi Clearance Predominantly through Enhanced Innate Immune Responses J. Immunol., November 15, 2006; 177(10): 7076 - 7085. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. J. GLICKSTEIN and J. L. COBURN ASSOCIATION OF MACROPHAGE INFLAMMATORY RESPONSE AND CELL DEATH AFTER IN VITRO BORRELIA BURGDORFERI INFECTION WITH ARTHRITIS RESISTANCE Am J Trop Med Hyg, November 1, 2006; 75(5): 964 - 967. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. W. Barthold, E. Hodzic, S. Tunev, and S. Feng Antibody-mediated disease remission in the mouse model of lyme borreliosis. Infect. Immun., August 1, 2006; 74(8): 4817 - 4825. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. R. Montgomery, K. Schreck, X. Wang, and S. E. Malawista Human Neutrophil Calprotectin Reduces the Susceptibility of Borrelia burgdorferi to Penicillin Infect. Immun., April 1, 2006; 74(4): 2468 - 2472. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
