Evidence map›Paper›PMID 26438793›Full record

ArticleInfection and immunity2015

Outer surface protein OspC is an antiphagocytic factor that protects Borrelia burgdorferi from phagocytosis by macrophages.

Sebastian E Carrasco, Bryan Troxell, Youyun Yang, Stephanie L Brandt, Hongxia Li, George E Sandusky, Keith W Condon, C Henrique Serezani, X Frank Yang

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.2field-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

52 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Characterization ofMicroorganisms · 2026
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  3. Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026
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  5. Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025
    Review
  6. Article
  7. Infection and immunity · 2025
    Article
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  14. Differential Resistance ofPathogens (Basel, Switzerland) · 2023
    Article
  15. Review
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  19. Review
  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

9 authors at 2 institutions in 1 country.

Sebastian E CarrascoDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Bryan TroxellDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Youyun YangDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Stephanie L BrandtDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Hongxia LiDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
George E SanduskyDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Keith W CondonDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
C Henrique SerezaniDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA hserezan@iupui.edu xfyang@iupui.edu.
X Frank YangDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA hserezan@iupui.edu xfyang@iupui.edu.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

Immunology and Infectious Diseases Training ProgramT32AI060519 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MARK H KAPLAN · 2004 to 2026
$6.0M
Regulatory Network of the Lyme Disease PathogenR01AI083640 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI X. Frank Yang · 2009 to 2026
$5.9M
Phosphatase and tensin homolog PTEN actions in polymicrobial sepsisR01HL124159 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SEREZANI, C. HENRIQUE · 2014 to 2022
$4.2M
EXTRAMURAL RESEARCH FACILITIES CONSTRUCTIONC06RR015481 · NCRR · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIFE, ROSE S · 2001 to 2001
$1.6M
Regulation of Toll-like receptor-induced NFkB activation by Gai-coupled receptorsR00HL103777 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI SEREZANI, C. HENRIQUE · 2012 to 2014
$713k
Cyclic di-GMP-dependent regulation of metabolism and virulence in Borrelia burgdorferiR21AI117198 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI GOMELSKY, MARK, YANG, X. FRANK · 2015 to 2016
$429k
Regulation of Toll-like receptor-induced NFkB activation by Gai-coupled receptorsK99HL103777 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SEREZANI, C. HENRIQUE · 2010 to 2011
$242k
NCRR NIH HHS C06 RR015481NCRR NIH HHS C06 RR015481-01NHLBI NIH HHS HL-103777NHLBI NIH HHS HL-124159NHLBI NIH HHS K99 HL103777NHLBI NIH HHS R00 HL103777NHLBI NIH HHS R01 HL124159NIAID NIH HHS 1R21AI117198NIAID NIH HHS 2R01AI083640NIAID NIH HHS R01 AI083640NIAID NIH HHS R21 AI117198NIAID NIH HHS T32 AI 060519NIAID NIH HHS T32 AI060519
6 · The paper itself

Abstract

Outer surface protein C (OspC) is one of the major lipoproteins expressed on the surface of Borrelia burgdorferi during tick feeding and the early phase of mammalian infection. OspC is required for B. burgdorferi to establish infection in both immunocompetent and SCID mice and has been proposed to facilitate evasion of innate immune defenses. However, the exact biological function of OspC remains elusive. In this study, we showed that the ospC-deficient spirochete could not establish infection in NOD-scid IL2rγ(null) mice that lack B cells, T cells, NK cells, and lytic complement. The ospC mutant also could not establish infection in anti-Ly6G-treated SCID and C3H/HeN mice (depletion of neutrophils). However, depletion of mononuclear phagocytes at the skin site of inoculation in SCID and C3H/HeN mice allowed the ospC mutant to establish infection in vivo. In phagocyte-depleted mice, the ospC mutant was able to colonize the joints and triggered neutrophilia during dissemination. Furthermore, we found that phagocytosis of green fluorescent protein (GFP)-expressing ospC mutant spirochetes by murine peritoneal macrophages and human THP-1 macrophage-like cells, but not in PMN-HL60, was significantly higher than parental wild-type B. burgdorferi strains, suggesting that OspC has an antiphagocytic property. In addition, overproduction of OspC in spirochetes also decreased the uptake of spirochetes by murine peritoneal macrophages. Together, our findings provide evidence that mononuclear phagocytes play a key role in clearance of the ospC mutant and that OspC promotes spirochetes' evasion of macrophages during early Lyme borreliosis.

Indexed as

Gene Expression Regulation, BacterialImmune EvasionAnimalsAntigens, BacterialBacterial Outer Membrane ProteinsB-LymphocytesBorrelia burgdorferiCell LineFemaleGenes, ReporterGreen Fluorescent ProteinsHumansKiller Cells, NaturalLyme DiseaseMacrophages, PeritonealMiceAntigens, BacterialBacterial Outer Membrane ProteinsGreen Fluorescent ProteinsOspC protein

Identifiers

PMID26438793
PMCPMC4645385
OpenAlexW2220103277

What OpenQuestion holds

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Registered trials

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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.