ArticleInfection and immunity2008
The failure of immune response evasion by linear plasmid 28-1-deficient Borrelia burgdorferi is attributable to persistent expression of an outer surface protein.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Mostly getting along -Borrelia burgdorferi and its manipulation of the host immune system.ImmunoHorizons · 2026Review
- Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025Review
- Diverse plasmid systems and their ecology across human gut metagenomes revealed by PlasX and MobMess.Nature microbiology · 2024Article
- Immune Response toCurrent issues in molecular biology · 2021Article
- Detecting Borrelia Spirochetes: A Case Study With Validation Among Autopsy Specimens.Frontiers in neurology · 2021Article
- Primordial origin and diversification of plasmids in Lyme disease agent bacteria.BMC genomics · 2018Article
- Plasmid diversity and phylogenetic consistency in the Lyme disease agent Borrelia burgdorferi.BMC genomics · 2017Article
- Review
- Investigating the potential role of non-vls genes on linear plasmid 28-1 in virulence and persistence by Borrelia burgdorferi.BMC microbiology · 2016Article
- Antigenic Variation in Bacterial Pathogens.Microbiology spectrum · 2016Article
- Role of the VlsE Lipoprotein in Immune Avoidance by the Lyme Disease SpirocheteForum on immunopathological diseases and therapeutics · 2016Article
- Presence of Arp specifically contributes to joint tissue edema associated with early-onset Lyme arthritis.Infection and immunity · 2014Article
- Lipoprotein succession in Borrelia burgdorferi: similar but distinct roles for OspC and VlsE at different stages of mammalian infection.Molecular microbiology · 2013Article
- Repression of bacterial lipoprotein production by Francisella novicida facilitates evasion of innate immune recognition.Cellular microbiology · 2012Article
- Genome stability of Lyme disease spirochetes: comparative genomics of Borrelia burgdorferi plasmids.PloS one · 2012Article
- Persistence of Borrelia burgdorferi in rhesus macaques following antibiotic treatment of disseminated infection.PloS one · 2012Article
- Regulation of the virulence determinant OspC by bbd18 on linear plasmid lp17 of Borrelia burgdorferi.Journal of bacteriology · 2011Article
- CsrA modulates levels of lipoproteins and key regulators of gene expression critical for pathogenic mechanisms of Borrelia burgdorferi.Infection and immunity · 2011Article
- Overexpression of CsrA (BB0184) alters the morphology and antigen profiles of Borrelia burgdorferi.Infection and immunity · 2009Article
- OspC-independent infection and dissemination by host-adapted Borrelia burgdorferi.Infection and immunity · 2009Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infectivity and persistence by Borrelia burgdorferi, the etiologic agent of Lyme disease, rely stringently on regulatory events. Among these is the downregulation of lipoprotein antigen expression, exemplified by outer surface protein C (OspC), at the advent of specific immunity in the mammalian host. B. burgdorferi spirochetes that lack the linear plasmid 28-1 (lp28-1) succumb to the host's immune response. We thus explored the notion that these two phenomena were related--that lp28-1(-) organisms fail to downregulate ospC and thus are cleared following the appearance of anti-OspC antibody in the murine host. The lp-28-1(-) isolate and a wild-type (wt) isolate bearing the complete set of plasmids were grown in dialysis membrane chambers that were implanted into rat peritoneal cavities. Analysis of mRNA and protein from these cultures showed that OspC expression levels by lp28-1(-) organisms are abnormally high in vivo. A time course analysis of ospC expression in tissues following infection indicates also that temporal diminution of the dominant antigen OspC is impaired in lp28-1(-) spirochetes. Finally, passive transfer of monoclonal OspC-specific antibody into SCID mice 8 days postinfection cleared lp28-1(-) spirochetes, yet the wt organisms persisted in a majority of animals. These findings indicate that incomplete repression of OspC by lp28-1(-) organisms renders them susceptible to immune-mediated clearance. The lp28-1 plasmid must harbor one or more genes involved in OspC downregulation.
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