Evidence map›Paper›PMID 18809667›Full record

ArticleInfection and immunity2008

Borrelia burgdorferi lacking DbpBA exhibits an early survival defect during experimental infection.

Eric H Weening, Nikhat Parveen, Jerome P Trzeciakowski, John M Leong, Magnus Höök, Jonathan T Skare

Open access · greenAbstract read
In one paragraph

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 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

91 citing papers in PubMed, 115 citations in OpenAlex.

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  15. Genetic Manipulation ofCurrent issues in molecular biology · 2021
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  16. Live Imaging.Current issues in molecular biology · 2021
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  17. Lyme Disease in Humans.Current issues in molecular biology · 2021
    Article
  18. Lyme Disease Pathogenesis.Current issues in molecular biology · 2021
    Review
  19. Interactions between Borrelia burgdorferi and ticks.Nature reviews. Microbiology · 2020
    Review
  20. Article

31 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Eric H WeeningDepartment of Microbial and Molecular Pathogenesis, College of Medicine, Texas A&M Health Science Center, College Station, TX 77843, USA.
Nikhat Parveen
Jerome P Trzeciakowski
John M Leong
Magnus Höök
Jonathan T Skare
Texas A&M Health Science Center · USUniversity of Massachusetts Chan Medical School · 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
Host Spirochete Interactions in Lyme DiseaseR01AI058086 · NIAID · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI SKARE, JON T · 2006 to 2010
$1.8M
DbpA/B proteins of Borrelia burgdorferi &Lyme arthritisR03AR049383 · NIAMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI PARVEEN, NIKHAT · 2003 to 2005
$237k
NIAID NIH HHS R01 AI037601NIAID NIH HHS R01-AI037601NIAID NIH HHS R01 AI058086NIAID NIH HHS R01-AI058086NIAMS NIH HHS R03 AR049383NIAMS NIH HHS R03-AR049383
6 · The paper itself

Abstract

Several Borrelia burgdorferi genes induced under mammalian host conditions have been purported to be important in Lyme disease pathogenesis based on their binding to host structures. These genes include the dbpBA locus, whose products bind host decorin and glycosoaminoglycans. Recently, the dbpBA genes were reported to be involved in borrelial infectivity. Here we extended the previous observations by using culture and quantitative PCR to evaluate low- and high-dose murine infection by a Delta dbpBA::Gent(r) derivative of B. burgdorferi strain B31. The results indicate that the Delta dbpBA::Gent(r) mutant is attenuated in the ability to initially colonize and then persist in multiple tissues. The mutant exhibited a colonization defect as early as 3 days postinfection, before the development of an adaptive immune response, and after low-dose infection of SCID mice, which are deficient in adaptive immunity. These findings suggest that the inability to adhere to host decorin may promote clearance of B. burgdorferi, presumably via innate immune mechanisms. In a high-dose infection, the mutant disseminated to several tissues, particularly joint tissue, but it was generally cleared from these tissues by 3 weeks postinfection. Finally, following high-dose infection of SCID mice, the dbpBA mutant exhibited only a mild colonization defect, suggesting that the adaptive response is involved in the clearance of the mutant in immunocompetent mice. Taken together, these results suggest that the DbpBA proteins facilitate the colonization of multiple tissues by B. burgdorferi and are required for optimal resistance to both innate and adaptive immune mechanisms following needle inoculation.

Indexed as

Adhesins, BacterialAnimalsBlotting, WesternBorrelia burgdorferiDecorinExtracellular Matrix ProteinsLyme DiseaseMiceMice, SCIDPolymerase Chain ReactionProteoglycansAdhesins, BacterialDcn protein, mouseDdpB protein, Borrelia burgdorferiDecorinExtracellular Matrix ProteinsProteoglycans

Identifiers

PMID18809667
PMCPMC2583571
OpenAlexW2135278450

What OpenQuestion holds

Textmetadata
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.