[New aspects of pathogenesis of Lyme borreliosis].
B. burgdorferi can evade the destructive effects of the immune system by binding host's complement regulators, which leads to inhibition of the complement activation cascade. Complement activity is blocked by CRASPs--complement regulator acquiring surface proteins. Complement resistance might therefore represent one major pathogenic factor favoring spirochete transmission to the vertebrate host, as well as determine host reservoirs of Borrelia burgdorferi genospecies. The cause of neuro-psychiatric disorders developing in some patients with Lyme borreliosis is still unknown. One of the hypotheses links them to neuro-hormonal disturbances induced by B. burgdorferi infection.
Zajkowska
Joanna
J
Klinika Chorób Zakaźnych i Neuroinfekcji AM w Białymstoku.
Grygorczuk
Sambor
S
Kondrusik
Maciej
M
Pancewicz
Sławomir
S
Hermanowska-Szpakowicz
Teresa
T
D000818:Animals; D001425:Bacterial Outer Membrane Proteins / Q000378:metabolism*; D001426:Bacterial Proteins / Q000378:metabolism*; D025065:Borrelia burgdorferi / Q000472:pathogenicity*; D003167:Complement Activation / Q000276:immunology; D006801:Humans; D008193:Lyme Disease / Q000276:immunology* / Q000382:microbiology*; D020852:Lyme Neuroborreliosis / Q000276:immunology; D008565:Membrane Proteins / Q000276:immunology; D013045:Species Specificity
D001425:Bacterial Outer Membrane Proteins; D001426:Bacterial Proteins; D008565:Membrane Proteins