Abstract
Many pathogenic microorganisms express fibronectin-binding molecules that facilitate their adherence to the extracellular matrix and/or entry into mammalian cells. We have previously described a Borrelia recurrentis gene, cihC that encodes a 40-kDa surface receptor for both, fibronectin and the complement inhibitors C4bp and C1-Inh. We now provide evidence for the expression of a group of highly homologues surface proteins, termed FbpA, in three B. hermsii isolates and two tick-borne relapsing fever spirochetes, B. parkeri and B. turicatae. When expressed in Escherichia coli or B. burgdorferi, four out of five proteins were shown to selectively bind fibronectin, whereas none of five proteins were able to bind the human complement regulators, C4bp and C1-Inh. By applying deletion mutants of the B. hermsii fibronectin-binding proteins a putative high-affinity binding site for fibronectin was mapped to its central region. In addition, the fibronectin-binding proteins of B. hermsii were found to share sequence homology with BBK32 of the Lyme disease spirochete B. burgdorferi with similar function suggesting its involvement in persistence and/or virulence of relapsing fever spirochetes.
Highlights
B. hermsii, the causative agent of tick-borne relapsing fever is transmitted to humans through the bite of its infected argasid tick vector, Ornithordoros hermsi [1]
Previous experiments have shown that the louse-borne relapsing fever spirochete B. recurrentis and the African tick-borne spirochete B. duttonii bind the human complement regulators C4bp and C1-Inh as well as fibronectin via their outer surface lipoprotein CihC
Screening for C4bp and fibronectin binding, employing cell lysates derived from North American tick-borne relapsing fever spirochete species B. hermsii, B. parkeri and B. turicatae either Ponceaus S stained or immunoblotted as depicted in Fig. 1 revealed that with the exception of B. recurrentis all other strains of tick-borne relapsing fever Borrelia as well as Lyme disease spirochetes (B. burgdorferi strain ZS7, B. garinii strain ZQ1 and B. afzelii strain MMS) failed to express C4bp-binding molecules (Fig. 1A)
Summary
B. hermsii, the causative agent of tick-borne relapsing fever is transmitted to humans through the bite of its infected argasid tick vector, Ornithordoros hermsi [1]. Isolates FRO and HS1 belonging to GGI and YOR to GGII were shown to be distinct from isolates of B. turicatae and B. parkeri spirochetes [6,7,8]. B. hermsii have evolved several strategies to persist in hosts and to evade innate and adaptive immunity, including antigenic variation, as seen for Vmp proteins [9,10,11] and specific binding, via cell surface receptors, of host derived complement regulators [12,13,14,15]. B. hermsii as well as other spirochetes, including B. burgdorferi, the causal agent of Lyme disease and the louse-borne relapsing fever spirochete B. recurrentis, were shown to bind and exploit functional active host-derived proteases, e.g. human plasminogen, to facilitate immune evasion and/or persistence [12,17,18,19]
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