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2017 ; 8
(ä): 328
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There Is a Method to the Madness: Strategies to Study Host Complement Evasion by
Lyme Disease and Relapsing Fever Spirochetes
#MMPMID28303129
Marcinkiewicz AL
; Kraiczy P
; Lin YP
Front Microbiol
2017[]; 8
(ä): 328
PMID28303129
show ga
Lyme disease and relapsing fever are caused by various Borrelia species. Lyme
disease borreliae, the most common vector-borne pathogens in both the U.S. and
Europe, are transmitted by Ixodes ticks and disseminate from the site of tick
bites to tissues leading to erythema migrans skin rash, arthritis, carditis, and
neuroborreliosis. Relapsing fever borreliae, carried by ticks and lice, trigger
reoccurring fever episodes. Following transmission, spirochetes survive in the
blood to induce bacteremia at the early stages of infection, which is thought to
promote evasion of the host complement system. The complement system acts as an
important innate immune defense mechanism in humans and vertebrates. Upon
activation, the cleaved complement components form complexes on the pathogen
surface to eventually promote bacteriolysis. The complement system is negatively
modulated by a number of functionally diverse regulators to avoid tissue damage.
To evade and inhibit the complement system, spirochetes are capable of binding
complement components and regulators. Complement inhibition results in bacterial
survival in serum (serum resistance) and is thought to promote bloodstream
survival, which facilitates spirochete dissemination and disease manifestations.
In this review, we discuss current methodologies to elucidate the mechanisms of
Borrelia spp. that promote serum resistance and bloodstream survival, as well as
novel methods to study factors responsible for bloodstream survival of Lyme
disease borreliae that can be applied to relapsing fever borreliae. Understanding
the mechanisms these pathogens utilize to evade the complement system will
ultimately aid in the development of novel therapeutic strategies and disease
prevention to improve human health.