Open AccessImpaired host defense to infection and Toll‐like receptor 2‐independent killing of Borrelia burgdorferi clinical isolates in TLR2‐deficient C3H/HeJ mice
Author(s) -
Wang Guiqing,
Ma Ying,
Buyuk Arzu,
McClain Steve,
Weis Janis J,
Schwartz Ira
Publication year - 2004
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1016/s0378-1097(03)00960-1
Subject(s) - borrelia burgdorferi , tlr2 , microbiology and biotechnology , toll like receptor , host (biology) , biology , virology , spirochaetaceae , borrelia burgdorferi infection , borrelia , immunology , tlr4 , innate immune system , immune system , antibody , ecology
To investigate the role of Toll‐like receptor 2 (TLR2)‐mediated signaling in host innate defense and development of Lyme disease, the pathogenicity of Borrelia burgdorferi sensu stricto clinical isolates representing two distinct genotypes (RST1 and RST3A) was assessed in TLR2 −/− C3H/HeJ mice. All TLR2 −/− mice infected with a B. burgdorferi RST1 isolate developed severe arthritis. The numbers of spirochetes in heart, joint and ear biopsy specimens were significantly higher in TLR2 −/− mice than in wild‐type mice similarly infected as determined by real‐time quantitative polymerase chain reaction. Interestingly, despite the higher spirochete levels in heart tissues, milder carditis was observed in TLR2 −/− than in wild‐type mice infected with this RST1 isolate ( P =0.02 ). By contrast, no positive cultures were obtained from any of the blood and tissue specimens from TLR2 −/− mice inoculated with two RST3A clinical isolates. The data suggest that there is impaired host innate defense against infection and TLR2‐independent killing of B. burgdorferi clinical isolates in TLR2‐deficient C3H/HeJ mice.