Borrelia burgdorferi regulates expression of complement regulator-acquiring surface protein 1 during the mammal-tick infection cycle.
During the natural mammal-tick infection cycle, the Lyme disease spirochete Borrelia burgdorferi comes into contact with components of the alternative complement pathway. B. burgdorferi, like many other human pathogens, has evolved the immune evasion strategy of binding two host-derived fluid-phase regulators of complement, factor H and factor H-like protein 1 (FHL-1). The borrelial complement regulator-acquiring surface protein 1 (CRASP-1) is a surface-exposed lipoprotein that binds both factor H and FHL-1. Analysis of CRASP-1 expression during the mammal-tick infectious cycle indicated that B. burgdorferi expresses this protein during mammalian infection, supporting the hypothesized role for CRASP-1 in immune evasion. However, CRASP-1 synthesis was repressed in bacteria during colonization of vector ticks. Analysis of cultured bacteria indicated that CRASP-1 is differentially expressed in response to changes in pH. Comparisons of CRASP-1 expression patterns with those of other infection-associated B. burgdorferi proteins, including the OspC, OspA, and Erp proteins, indicated that each protein is regulated through a unique mechanism.
von Lackum
Kate
K
Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, MS417 Chandler Medical Center, 800 Rose Street, Lexington, KY 40536-0298, USA.
Miller
Jennifer C
JC
Bykowski
Tomasz
T
Riley
Sean P
SP
Woodman
Michael E
ME
Brade
Volker
V
Kraiczy
Peter
P
Stevenson
Brian
B
Wallich
Reinhard
R
D000818:Animals; D001426:Bacterial Proteins / Q000096:biosynthesis*; D001798:Blood Proteins / Q000737:chemistry; D025065:Borrelia burgdorferi / Q000502:physiology*; D003180:Complement C3b Inactivator Proteins; D017242:Complement Factor H / Q000737:chemistry; D019143:Evolution, Molecular; D005260:Female; D015964:Gene Expression Regulation, Bacterial; D006863:Hydrogen-Ion Concentration; D007814:Larva; D008193:Lyme Disease / Q000382:microbiology; D008297:Male; D008322:Mammals / Q000469:parasitology*; D008565:Membrane Proteins / Q000096:biosynthesis*; D051379:Mice; D008807:Mice, Inbred BALB C; D009758:Nymph; D011817:Rabbits; D013987:Ticks / Q000382:microbiology* / Q000502:physiology
D001426:Bacterial Proteins; D001798:Blood Proteins; C517621:CFHR1 protein, human; D003180:Complement C3b Inactivator Proteins; D008565:Membrane Proteins; C440651:complement regulator-acquiring surface proteins, Borrelia burgdorferi; D017242:Complement Factor H