Evidence map›Paper›PMID 32413091›Full record

ArticlePLoS pathogens2020

Strain-specific joint invasion and colonization by Lyme disease spirochetes is promoted by outer surface protein C.

Yi-Pin Lin, Xi Tan, Jennifer A Caine, Mildred Castellanos, George Chaconas, Jenifer Coburn, John M Leong

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Lyme borreliosis.Nature reviews. Disease primers · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025
    Review
  9. Article
  10. Article
  11. Pathogens (Basel, Switzerland) · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Differential Resistance ofPathogens (Basel, Switzerland) · 2023
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Yi-Pin LinDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.ORCID 0000-0002-5240-2031
Xi TanDepartments of Biochemistry & Molecular Biology and Microbiology, Immunology & Infectious Diseases, Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.ORCID 0000-0002-8128-9082
Jennifer A CaineDivision of Infectious Diseases, and Center for Infectious Disease Research, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.ORCID 0000-0002-7649-0267
Mildred CastellanosDepartments of Biochemistry & Molecular Biology and Microbiology, Immunology & Infectious Diseases, Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.
George ChaconasDepartments of Biochemistry & Molecular Biology and Microbiology, Immunology & Infectious Diseases, Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.ORCID 0000-0002-9611-2095
Jenifer CoburnDivision of Infectious Diseases, and Center for Infectious Disease Research, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.ORCID 0000-0001-6460-2017
John M LeongDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.ORCID 0000-0003-0240-6402
University of Calgary · CAMedical College of Wisconsin · USTufts University · US

Funding

PROTEOGLYCAN BINDING BY A B BURGDORFERI HEMAGGLUTININR01AI037601 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LEONG, JOHN M · 1995 to 2010
$3.6M
Functional Analyses of Borrelia burgdorferi AdhesinsR01AI118799 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI CHACONAS, GEORGE, COBURN, JENIFER L · 2016 to 2020
$3.3M
Multiple B. burgdorferi Factors Collaborate to Evade Complement-Mediated DefensesR01AI121401 · NIAID · TUFTS UNIVERSITY BOSTON · PI COBURN, JENIFER L, LEONG, JOHN M · 2016 to 2020
$3.1M
NIAID NIH HHS R01 AI037601NIAID NIH HHS R01 AI118799NIAID NIH HHS R01 AI121401
6 · The paper itself

Abstract

Lyme disease, caused by Borrelia burgdorferi, B. afzelii and B. garinii, is a chronic, multi-systemic infection and the spectrum of tissues affected can vary with the Lyme disease strain. For example, whereas B. garinii infection is associated with neurologic manifestations, B. burgdorferi infection is associated with arthritis. The basis for tissue tropism is poorly understood, but has been long hypothesized to involve strain-specific interactions with host components in the target tissue. OspC (outer surface protein C) is a highly variable outer surface protein required for infectivity, and sequence differences in OspC are associated with variation in tissue invasiveness, but whether OspC directly influences tropism is unknown. We found that OspC binds to the extracellular matrix (ECM) components fibronectin and/or dermatan sulfate in an OspC variant-dependent manner. Murine infection by isogenic B. burgdorferi strains differing only in their ospC coding region revealed that two OspC variants capable of binding dermatan sulfate promoted colonization of all tissues tested, including joints. However, an isogenic strain producing OspC from B. garinii strain PBr, which binds fibronectin but not dermatan sulfate, colonized the skin, heart and bladder, but not joints. Moreover, a strain producing an OspC altered to recognize neither fibronectin nor dermatan sulfate displayed dramatically reduced levels of tissue colonization that were indistinguishable from a strain entirely deficient in OspC. Finally, intravital microscopy revealed that this OspC mutant, in contrast to a strain producing wild type OspC, was defective in promoting joint invasion by B. burgdorferi in living mice. We conclude that OspC functions as an ECM-binding adhesin that is required for joint invasion, and that variation in OspC sequence contributes to strain-specific differences in tissue tropism displayed among Lyme disease spirochetes.

Indexed as

AnimalsAntigens, BacterialBacterial AdhesionBacterial Outer Membrane ProteinsBorrelia burgdorferiDermatan SulfateExtracellular MatrixFemaleFibronectinsJoint DiseasesJointsLyme DiseaseMiceMice, SCIDMutationOrgan SpecificityAntigens, BacterialBacterial Outer Membrane ProteinsDermatan SulfateFibronectinsOspC protein

Identifiers

PMID32413091
PMCPMC7255614
OpenAlexW3025805039

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.