ArticleThe American journal of pathology2011
Borrelia burgdorferi RST1 (OspC type A) genotype is associated with greater inflammation and more severe Lyme disease.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 139 citations in OpenAlex.
- Mostly getting along -Borrelia burgdorferi and its manipulation of the host immune system.ImmunoHorizons · 2026Review
- Curiouser and curiouser: understanding the intersection of inter- and intra-specific diversity during theInfection and immunity · 2026Review
- Developing a durable, memory-driven, CspZ-targeting Lyme disease vaccine by rational adjuvant selection.NPJ vaccines · 2026Article
- Innate immune responses tomBio · 2026Article
- Lyme borreliosis.Nature reviews. Disease primers · 2026Review
- Oxford nanopore technology R10 improved assembly metrics of Borrelia plasmids compared to R9.BMC genomics · 2026Article
- Evaluation of immunoreactive epitopes in the sera and cerebrospinal fluid of patients with post-treatment Lyme disease syndrome.Scientific reports · 2026Article
- Develop a durable, memory-driven, CspZ-targeting Lyme disease vaccine by rationale adjuvant selection.bioRxiv : the preprint server for biology · 2026Article
- Polyvalent mRNA vaccine targeting outer surface protein C affords multi-strain protection against Lyme disease.NPJ vaccines · 2025Article
- Genomic characterization of clinical Borrelia burgdorferi sensu lato isolates in the Netherlands over a thirty-year period.BMC genomics · 2025Article
- Mechanistic insights into the structure-based design of a CspZ-targeting Lyme disease vaccine.Nature communications · 2025Article
- Complex exchanges among plasmids and clonal expansion of lineages shape the population structure and virulence ofbioRxiv : the preprint server for biology · 2025Article
- Toll-like receptor 1 polymorphism is associated with impaired immune tolerance, dysregulated inflammatory responses toFrontiers in immunology · 2025Article
- Mesenchymal Stem Cells Reduce Inflammation in a Mouse Model of Lyme Arthritis.Stem cells international · 2025Article
- CspZ variant-specific interaction with factor H incorporates a metal site to support Lyme borreliae complement evasion.The Journal of biological chemistry · 2025Article
- Borrelia PeptideAtlas: A proteome resource of common Borrelia burgdorferi isolates for Lyme research.Scientific data · 2024Article
- Bridging the gap: Insights in the immunopathology of Lyme borreliosis.European journal of immunology · 2024Review
- Microbial genetic variation impacts host eco-immunological strategies and microparasite fitness in Lyme borreliae-reptile system.Ticks and tick-borne diseases · 2024Article
- Lyme Arthritis: A 50-Year Journey.The Journal of infectious diseases · 2024Article
- Analysis of the Borreliaceae Pangenome Reveals a Distinct Genomic Architecture Conserved Across Phylogenetic Scales.The Journal of infectious diseases · 2024Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Evidence is emerging for differential pathogenicity among Borrelia burgdorferi genotypes in the United States. By using two linked genotyping systems, ribosomal RNA intergenic spacer type (RST) and outer surface protein C (OspC), we studied the inflammatory potential of B. burgdorferi genotypes in cells and patients with erythema migrans or Lyme arthritis. When macrophages were stimulated with 10 isolates of each RST1, RST2, or RST3 strain, RST1 (OspC type A)-stimulated cells expressed significantly higher levels of IL-6, IL-8, chemokine ligand (CCL) 3, CCL4, tumor necrosis factor, and IL-1β, factors associated with innate immune responses. In peripheral blood mononuclear cells, RST1 strains again stimulated significantly higher levels of these mediators. Moreover, compared with RST2, RST1 isolates induced significantly more interferon (IFN)-α, IFN-γ, and CXCL10, which are needed for adaptive immune responses; however, OspC type I (RST3) approached RST1 (OspC type A) in stimulating these adaptive immune mediators. Similarly, serum samples from patients with erythema migrans who were infected with the RST1 genotype had significantly higher levels of almost all of these mediators, including exceptionally high levels of IFN-γ-inducible chemokines, CCL2, CXCL9, and CXCL10; and this pronounced inflammatory response was associated with more symptomatic infection. Differences among genotypes were not as great in patients with Lyme arthritis, but those infected with RST1 strains more often had antibiotic-refractory arthritis. Thus, the B. burgdorferi RST1 (OspC type A) genotype, followed by the RST3 (OspC type I) genotype, causes greater inflammation and more severe disease, establishing a link between spirochetal virulence and host inflammation.
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