Abstract
Spirochetes belonging to the Borrelia (B.) burgdorferi sensu lato complex differ in their resistance to complement-mediated killing, particularly in regard to human serum. In the present study, we elucidate the serum and complement susceptibility of B. valaisiana, a genospecies with the potential to cause Lyme disease in Europe as well as in Asia. Among the investigated isolates, growth of ZWU3 Ny3 was not affected while growth of VS116 and Bv9 was strongly inhibited in the presence of 50% human serum. Analyzing complement activation, complement components C3, C4 and C6 were deposited on the surface of isolates VS116 and Bv9, and similarly the membrane attack complex was formed on their surface. In contrast, no surface-deposited components and no aberrations in cell morphology were detected for serum-resistant ZWU3 Ny3. While further investigating the protective role of bound complement regulators in mediating complement resistance, we discovered that none of the B. valaisiana isolates analyzed bound complement regulators Factor H, Factor H-like protein 1, C4b binding protein or C1 esterase inhibitor. In addition, B. valaisiana also lacked intrinsic proteolytic activity to degrade complement components C3, C3b, C4, C4b, and C5. Taken together, these findings suggest that certain B. valaisiana isolates differ in their capability to resist complement-mediating killing by human serum. The molecular mechanism utilized by B. valaisiana to inhibit bacteriolysis appears not to involve binding of the key host complement regulators of the alternative, classical, and lectin pathways as already known for serum-resistant Lyme disease or relapsing fever borreliae.
Highlights
Lyme disease, the most prevalent vector-borne anthropozoonosis in Europe and North America is caused by spirochetes belonging to the Borrelia (B.) burgdorferi sensu lato (s.l.) complex [1]
Serum Susceptibility of B. valaisiana To further evaluate the serum resistance pattern of B. valaisiana to human complement, three isolates collected from ticks at different geographical locations were incubated in 50% active Normal human serum (NHS) or in 50% heat-inactivated human serum (hiNHS) for up to 9 days and cell growth was monitored in a colorimetric growth survival assay [47,48]
As demonstrated in figure 1, growth of B. valaisiana isolate Bv9, B. valaisiana type strain VS116, and serumsensitive control strain B. garinii G1 when challenged with 50% NHS was completely inhibited as evidenced by only minor changes of absorbance values
Summary
The most prevalent vector-borne anthropozoonosis in Europe and North America is caused by spirochetes belonging to the Borrelia (B.) burgdorferi sensu lato (s.l.) complex [1]. In Central Europe, B. burgdorferi, B. afzelii, B. garinii, B. spielmanii as well as B. bavariensis are the causative agents of Lyme disease while the pathogenic potential for B. valaisiana remains unclear [2,3,4,5,6]. There are several lines of evidence that B. valaisiana (formely described as genomic groups VS116 and M19) might cause human Lyme disease even though only skin biopsies or cerebrospinal fluid samples of erythema migrans, acrodermatits chronica atrophicans, and neuroborreliosis patients were found to be positive for B. valaisiana DNA [3,4]. Progression of the cascade and formation of the lytic membrane attack complex (MAC) results in complement-mediated killing of the invading pathogen
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