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Relapsing fever Spirochetes Borrelia recurrentis and B. duttonii acquire complement regulators C4b-binding protein and factor H

Meri, T ; Cutler, SJ ; Blom, Anna LU orcid ; Meri, S and Jokiranta, TS (2006) In Infection and Immunity 74(7). p.4157-4163
Abstract
Relapsing fever is a rapidly progressive and severe septic disease caused by certain Borrelia spirochetes. The disease is divided into two forms, i.e., epidemic relapsing fever, caused by Borrelia recurrentis and transmitted by lice, and the endemic form, caused by several Borrelia species, such as B. duttonii, and transmitted by soft-bodied ticks. The spirochetes enter the bloodstream by the vector bite and live persistently in plasma even after the development of specific antibodies. This leads to fever relapses and high mortality and clearly indicates that the Borrelia organisms utilize effective immune evasion strategies. In this study, we show that the epidemic relapsing fever pathogen B. recurrentis and an endemic relapsing fever... (More)
Relapsing fever is a rapidly progressive and severe septic disease caused by certain Borrelia spirochetes. The disease is divided into two forms, i.e., epidemic relapsing fever, caused by Borrelia recurrentis and transmitted by lice, and the endemic form, caused by several Borrelia species, such as B. duttonii, and transmitted by soft-bodied ticks. The spirochetes enter the bloodstream by the vector bite and live persistently in plasma even after the development of specific antibodies. This leads to fever relapses and high mortality and clearly indicates that the Borrelia organisms utilize effective immune evasion strategies. In this study, we show that the epidemic relapsing fever pathogen B. recurrentis and an endemic relapsing fever pathogen, B. duttonii, are serum resistant, i.e., resistant to complement in vitro. They acquire the host alternative complement pathway regulator factor H on their surfaces in a similar way to that of the less serum-resistant Lyme disease pathogen, B. burgdorferi sensu stricto. More importantly, the relapsing fever spirochetes specifically bind host C4b-binding protein, a major regulator of the antibody-mediated classical complement pathway. Both complement regulators retained their functional activities when bound to the surfaces of the spirochetes. In conclusion, this is the first report of complement evasion by Borrelia recurrentis and B. duttonii and the first report showing capture of C4b-binding protein by spirochetes. (Less)
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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Infection and Immunity
volume
74
issue
7
pages
4157 - 4163
publisher
American Society for Microbiology
external identifiers
  • pmid:16790790
  • wos:000238591800049
  • scopus:33745596147
  • pmid:16790790
ISSN
1098-5522
DOI
10.1128/IAI.00007-06
language
English
LU publication?
yes
id
ee8e3b44-ca93-4000-889e-82fc4db41780 (old id 686474)
date added to LUP
2016-04-01 12:09:25
date last changed
2020-11-24 01:20:12
@article{ee8e3b44-ca93-4000-889e-82fc4db41780,
  abstract     = {Relapsing fever is a rapidly progressive and severe septic disease caused by certain Borrelia spirochetes. The disease is divided into two forms, i.e., epidemic relapsing fever, caused by Borrelia recurrentis and transmitted by lice, and the endemic form, caused by several Borrelia species, such as B. duttonii, and transmitted by soft-bodied ticks. The spirochetes enter the bloodstream by the vector bite and live persistently in plasma even after the development of specific antibodies. This leads to fever relapses and high mortality and clearly indicates that the Borrelia organisms utilize effective immune evasion strategies. In this study, we show that the epidemic relapsing fever pathogen B. recurrentis and an endemic relapsing fever pathogen, B. duttonii, are serum resistant, i.e., resistant to complement in vitro. They acquire the host alternative complement pathway regulator factor H on their surfaces in a similar way to that of the less serum-resistant Lyme disease pathogen, B. burgdorferi sensu stricto. More importantly, the relapsing fever spirochetes specifically bind host C4b-binding protein, a major regulator of the antibody-mediated classical complement pathway. Both complement regulators retained their functional activities when bound to the surfaces of the spirochetes. In conclusion, this is the first report of complement evasion by Borrelia recurrentis and B. duttonii and the first report showing capture of C4b-binding protein by spirochetes.},
  author       = {Meri, T and Cutler, SJ and Blom, Anna and Meri, S and Jokiranta, TS},
  issn         = {1098-5522},
  language     = {eng},
  number       = {7},
  pages        = {4157--4163},
  publisher    = {American Society for Microbiology},
  series       = {Infection and Immunity},
  title        = {Relapsing fever Spirochetes Borrelia recurrentis and B. duttonii acquire complement regulators C4b-binding protein and factor H},
  url          = {http://dx.doi.org/10.1128/IAI.00007-06},
  doi          = {10.1128/IAI.00007-06},
  volume       = {74},
  year         = {2006},
}