Survival of Borrelia burgdorferi Strain B31 in Human Serum Is Not Dependent on C4BP Binding to the Bacterial Surface

Lyme disease is a vector-borne illness caused by spirochetes belonging to the <i>Borrelia burgdorferi</i> species group. These bacteria employ several mechanisms to survive within the vertebrate host, including evasion of the complement system. In this study, we examine the protection against human serum killing by the binding of host complement regulators C4b-binding protein (C4BP) and factor H (FH) to the bacterial surface of <i>B. burgdorferi</i>. Via serum depletion of isolated complement regulators, we found that the absence of C4BP did not alter the survival of <i>B. burgdorferi</i> strain B31; however, the removal of FH increased the sensitivity of this strain to human serum as previously described. The <i>B. garinii</i> seabird-isolated strain Far04, on the other hand, did not bind any complement regulators of human origin and was serum-sensitive, indicating its special host species specificity.

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Publication Details

Journal
Pathogens
Published
2024-11-08
DOI
https://doi.org/10.3390/pathogens13110976
Primary Topic
Vector-borne infectious diseases
Type
article
Field-Weighted Citation Impact
0.00

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Survival of Borrelia burgdorferi Strain B31 in Human Serum Is Not Dependent on C4BP Binding to the Bacterial Surface

Sven Bergström, Tobias Jakobsson, Johan Normark, Pär Comstedt
Pathogens
Vector-borne infectious diseases
article

Survival of Borrelia burgdorferi Strain B31 in Human Serum Is Not Dependent on C4BP Binding to the Bacterial Surface

Sven Bergström, Tobias Jakobsson, Johan Normark, Pär Comstedt
article en

Abstract

Lyme disease is a vector-borne illness caused by spirochetes belonging to the <i>Borrelia burgdorferi</i> species group. These bacteria employ several mechanisms to survive within the vertebrate host, including evasion of the complement system. In this study, we examine the protection against human serum killing by the binding of host complement regulators C4b-binding protein (C4BP) and factor H (FH) to the bacterial surface of <i>B. burgdorferi</i>. Via serum depletion of isolated complement regulators, we found that the absence of C4BP did not alter the survival of <i>B. burgdorferi</i> strain B31; however, the removal of FH increased the sensitivity of this strain to human serum as previously described. The <i>B. garinii</i> seabird-isolated strain Far04, on the other hand, did not bind any complement regulators of human origin and was serum-sensitive, indicating its special host species specificity.

PathogensVol. 13(11)
ExpreS2ion Biotechnologies (Denmark) (DK), Umeå University (SE)
Vetenskapsrådet
Zero hunger
Openalex Percentile: Top 81%
Vector-borne infectious diseases
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