Borrelia Burgdorferi Detected in the Blood, Synovium and Skin of Patients with Lyme Arthritis

1994 ◽  
pp. 327-330
Author(s):  
Marika Valešová ◽  
Jana Hercogová ◽  
Dagmar Hulínská
Keyword(s):  
Borrelia Burgdorferi ◽  
Lyme Arthritis

scholarly journals Arthritis and Diagnostics in Lyme Disease

2021 ◽  
Vol 6 (1) ◽  
pp. 18
Author(s):  
Javier A. Quintero ◽  
Raluchukwu Attah ◽  
Reena Khianey ◽  
Eugenio Capitle ◽  
Steven E. Schutzer
Keyword(s):  
Lyme Disease ◽  
Borrelia Burgdorferi ◽  
Diagnostic Tests ◽  
Laboratory Tests ◽  
Diagnostic Methods ◽  
Lyme Arthritis ◽  
Differential Diagnoses ◽  
Antibody Testing ◽  
Active Infection ◽  
Indirect Measure

The diagnosis of Lyme disease, caused by Borrelia burgdorferi, is clinical but frequently supported by laboratory tests. Lyme arthritis is now less frequently seen than at the time of its discovery. However, it still occurs, and it is important to recognize this, the differential diagnoses, and how laboratory tests can be useful and their limitations. The most frequently used diagnostic tests are antibody based. However, antibody testing still suffers from many drawbacks and is only an indirect measure of exposure. In contrast, evolving direct diagnostic methods can indicate active infection.

Frequencies of Borrelia burgdorferi-reactive T lymphocytes in Lyme arthritis

1989 ◽  
Vol 9 (3-5) ◽  
pp. 237-241 ◽  
Author(s):  
A. Neumann ◽  
M. Schlesier ◽  
H. Schneider ◽  
A. Vogt ◽  
H. H. Peter
Keyword(s):  
T Lymphocytes ◽  
Borrelia Burgdorferi ◽  
Lyme Arthritis

scholarly journals Borrelia burgdorferi activates a T helper type 1-like T cell subset in Lyme arthritis.

1991 ◽  
Vol 174 (3) ◽  
pp. 593-601 ◽  
Author(s):  
H Yssel ◽  
M C Shanafelt ◽  
C Soderberg ◽  
P V Schneider ◽  
J Anzola ◽  
...  
Keyword(s):  
T Cell ◽  
Borrelia Burgdorferi ◽  
Cell Subset ◽  
Chronic Inflammatory Disease ◽  
T Cell Response ◽  
Lyme Arthritis ◽  
T Helper ◽  
Cell Clones ◽  
T Cell Lines

18 cloned T cell lines reactive with Borrelia burgdorferi proteins, all CD3+4+8-TCR-alpha/beta+ and restricted by HLA class II proteins, were isolated from four patients with chronic Lyme arthritis. Analysis of these T cell clones indicated that the T cell response to the Lyme disease spirochete is not oligoclonally restricted; yet all produced the same pattern of lymphokines, resembling that of murine type 1 T helper cells, after antigen-specific or nonspecific stimulation. Therefore, a subset of human CD4+ T cells, with a distinct profile of lymphokine secretion, is selectively activated by the pathogen inciting this chronic inflammatory disease.

Experimental Lyme Arthritis in Rats Infected with Borrelia burgdorferi

1988 ◽  
Vol 157 (4) ◽  
pp. 842-845 ◽  
Author(s):  
S. W. Barthold ◽  
K. D. Moody ◽  
G. A. Terwilliger ◽  
P. H. Duray ◽  
R. O. Jacoby ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Lyme Arthritis

scholarly journals Matrix Metalloproteinase 9 Plays a Key Role in Lyme Arthritis but Not in Dissemination of Borrelia burgdorferi

2009 ◽  
Vol 77 (7) ◽  
pp. 2643-2649 ◽  
Author(s):  
Andrew J. Heilpern ◽  
Warren Wertheim ◽  
Jia He ◽  
George Perides ◽  
Roderick T. Bronson ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Matrix Metalloproteinase ◽  
Type I Collagen ◽  
Insertion Site ◽  
Matrix Metalloproteinase 9 ◽  
Lyme Arthritis ◽  
Type I ◽  
Wild Type ◽  
Tissue Destruction ◽  
Metalloproteinase 9

ABSTRACT Borrelia burgdorferi, the causative agent of Lyme arthritis, does not produce any exported proteases capable of degrading extracellular matrix despite the fact that it is able to disseminate from a skin insertion site to infect multiple organs. Prior studies have shown that B. burgdorferi induces the host protease, matrix metalloproteinase 9 (MMP-9), and suggested that the induction of MMP-9 may allow the organism to disseminate and produce local tissue destruction. We examined the role of MMP-9 in dissemination of B. burgdorferi and pathogenesis of Lyme arthritis. In a MMP-9−/− mouse model, MMP-9 was not required for the dissemination of the spirochete to distant sites. However, MMP-9−/− exhibited significantly decreased arthritis compared to wild-type mice. The decrease in arthritis was not due to an inability to control infection since the spirochete numbers in the joints were identical. Levels of inflammatory chemokines and cytokines were also similar in MMP-9−/− and wild-type mice. We examined whether decreased inflammation in MMP-9−/− mice may be the result of decreased production of neoattractants by MMP-9-dependent cleavage of collagen. MMP-9 cleavage of type I collagen results in increased monocyte chemoattraction. MMP-9 plays an important role in regulating inflammation in Lyme arthritis, potentially through the cleavage of type I collagen.

scholarly journals Burden and viability of Borrelia burgdorferi in skin and joints of patients with erythema migrans or lyme arthritis

2011 ◽  
Vol 63 (8) ◽  
pp. 2238-2247 ◽  
Author(s):  
Xin Li ◽  
Gail A. McHugh ◽  
Nitin Damle ◽  
Vijay K. Sikand ◽  
Lisa Glickstein ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Erythema Migrans ◽  
Lyme Arthritis

scholarly journals Infection of Interleukin 17 Receptor A-Deficient C3H Mice with Borrelia burgdorferi Does Not Affect Their Development of Lyme Arthritis and Carditis

2015 ◽  
Vol 83 (7) ◽  
pp. 2882-2888 ◽  
Author(s):  
Carrie E. Lasky ◽  
Kara E. Jamison ◽  
Darcie R. Sidelinger ◽  
Carmela L. Pratt ◽  
Guoquan Zhang ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Lyme Borreliosis ◽  
Heart Tissue ◽  
Lyme Arthritis ◽  
Mouse Strains ◽  
Interleukin 17 ◽  
Content Type ◽  
C3h Mice ◽  
A Subunit

Recently, a number of studies have reported the presence of interleukin 17 (IL-17) in patients with Lyme disease, and several murine studies have suggested a role for this cytokine in the development of Lyme arthritis. However, the role of IL-17 has not been studied using the experimental Lyme borreliosis model of infection of C3H mice withBorrelia burgdorferi. In the current study, we investigated the role of IL-17 in the development of experimental Lyme borreliosis by infecting C3H mice devoid of the common IL-17 receptor A subunit (IL-17RA) and thus deficient in most IL-17 signaling. Infection of both C3H and C3H IL-17RA−/−mice led to the production of high levels of IL-17 in the serum, low levels in the heart tissue, and no detectable IL-17 in the joint tissue. The development and severity of arthritis and carditis in the C3H IL-17RA−/−mice were similar to what was seen in wild-type C3H mice. In addition, development of antiborrelia antibodies and clearance of spirochetes from tissues were similar for the two mouse strains. These results demonstrate a limited role for IL-17 signaling through IL-17RA in the development of disease following infection of C3H mice withB. burgdorferi.

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