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Feeding of Ticks on Animals for Transmission and Xenodiagnosis in Lyme Disease Research
Published on: August 31, 2013
[Immunopathology of Lyme arthritis]
Sławomir A Pancewicz1, Ryszard Rutkowski, Krzysztof Rutkowski
1Akademia Medyczna w Białymstoku, Klinika Chorób Zakaźnych i Neuroinfekcji. neuroin@amb.edu.pl
Abstract:
Lyme borreliosis (Lyme disease) is the most prevalent tick-borne disease caused by spirochaetes of the Borrelia species complex. Arthritis is one of the common manifestations of B. burgdorferi infection. The pathomechanism of articular changes in Lyme arthritis has not yet been elucidated. Histopathological studies of synovia and immunological changes are similar to rheumatoid arthritis. In the early stage of inflammation B. burgdorferi interact with polynuclear granulocytes and epithelial cells, triggering production of reactive oxygen species, lipid peroxidation products and other inflammatory mediators. The imbalance between anabolic and catabolic processes in inflamed joints results in the progressive destruction of articular cartilage and disintegration of extracellular matrix. Molecular mimicry between OspA (outer surface protein A) and adhesion molecule LFA-1alpha seems to be responsible for chronic arthritis.
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