Evidence map›Paper›PMID 23386602›Full record

ArticleThe Journal of biological chemistry2013

Autophagy modulates Borrelia burgdorferi-induced production of interleukin-1β (IL-1β).

Kathrin Buffen, Marije Oosting, Svenja Mennens, Paras K Anand, Theo S Plantinga, Patrick Sturm, Frank L van de Veerdonk, Jos W M van der Meer, Ramnik J Xavier, Thirumala-Devi Kanneganti and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  7. Uric acid priming in human monocytes is driven by the AKT-PRAS40 autophagy pathway.Proceedings of the National Academy of Sciences of the United States of America · 2017
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  16. Association of autophagy-related 16-like 1 (ATG16L1) gene polymorphism with sepsis severity in patients with sepsis and ventilator-associated pneumonia.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2014
    Article
  17. 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

12 authors at 4 institutions in 2 countries.

Kathrin BuffenDepartment of Medicine, Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands; Nijmegen Institute of Infection, Inflammation, and Immunity (N4i), Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands.
Marije OostingDepartment of Medicine, Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands; Nijmegen Institute of Infection, Inflammation, and Immunity (N4i), Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands.
Svenja MennensDepartment of Medicine, Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands; Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105.
Paras K AnandDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105.
Theo S PlantingaDepartment of Medicine, Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands; Nijmegen Institute of Infection, Inflammation, and Immunity (N4i), Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands.
Patrick SturmDepartment of Microbiology, Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands.
Frank L van de VeerdonkDepartment of Medicine, Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands; Nijmegen Institute of Infection, Inflammation, and Immunity (N4i), Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands.
Jos W M van der MeerDepartment of Medicine, Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands; Nijmegen Institute of Infection, Inflammation, and Immunity (N4i), Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands.
Ramnik J XavierGastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114.
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105.
Mihai G NeteaDepartment of Medicine, Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands; Nijmegen Institute of Infection, Inflammation, and Immunity (N4i), Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands.
Leo A B JoostenDepartment of Medicine, Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands; Nijmegen Institute of Infection, Inflammation, and Immunity (N4i), Radboud University Nijmegen Medical Centre, 6525 GA Nijmegen, The Netherlands. Electronic address: l.joosten@aig.umcn.nl.
Radboud University Medical Center · NLRadboud University Nijmegen · NLSt. Jude Children's Research Hospital · USMassachusetts General Hospital · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
Role of NLR Inflammasomes in Autoinflammatory Diseases and Host DefenseR01AR056296 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2008 to 2022
$5.9M
NIAMS NIH HHS R01 AR056296NIAMS NIH HHS R01AR056296NIDDK NIH HHS P30 DK043351
6 · The paper itself

Abstract

Borrelia burgdorferi sensu lato is the causative agent of Lyme disease. Recent studies have shown that recognition of the spirochete is mediated by TLR2 and NOD2. The latter receptor has been associated with the induction of the intracellular degradation process called autophagy. The present study demonstrated for the first time the induction of autophagy by exposure to B. burgdorferi and that autophagy modulates the B. burgdorferi-dependent cytokine production. Human peripheral blood mononuclear cells treated with autophagy inhibitors showed an increased IL-1β and IL-6 production in response to the exposure of the spirochete, whereas TNFα production was unchanged. Autophagy induction against B. burgdorferi was dependent on reactive oxygen species (ROS) because cells from patients with chronic granulomatous disease, which are defective in ROS production, also produced elevated IL-1β. Further, the enhanced production of the proinflammatory cytokines was because of the elevated mRNA expression in the absence of autophagy. Our results thus demonstrate the induction of autophagy, which, in turn, modulates cytokine production by B. burgdorferi for the first time.

Indexed as

AutophagyAdenineAndrostadienesBorrelia burgdorferiCaspase 1Cells, CulturedEnzyme ActivationHost-Pathogen InteractionsHumansInflammation MediatorsInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinInterleukin-6Leukocytes, MononuclearReactive Oxygen SpeciesReceptors, Interleukin-13-methyladenineAdenineAndrostadienesCaspase 1IL6 protein, humanInflammation MediatorsInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinInterleukin-6Reactive Oxygen SpeciesReceptors, Interleukin-1Tumor Necrosis Factor-alphaWortmannin

Identifiers

PMID23386602
PMCPMC3605684
OpenAlexW2098133447

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.