Evidence map›Paper›PMID 17517970›Full record

ArticleThe Journal of experimental medicine2007

Selective suppression of dendritic cell functions by Mycobacterium ulcerans toxin mycolactone.

Emmanuelle Coutanceau, Jeremie Decalf, Angelo Martino, Aurélie Babon, Nathalie Winter, Stewart T Cole, Matthew L Albert, Caroline Demangel

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
8.2field-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

64 citing papers in PubMed, 130 citations in OpenAlex.

  1. Trial
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  4. Observational
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  11. Pharmacologic management ofExpert review of clinical pharmacology · 2020
    Review
  12. Article
  13. In Vivo Imaging of BioluminescentThe American journal of tropical medicine and hygiene · 2019
    Article
  14. Article
  15. Article
  16. Article
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4 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

8 authors at 1 institution in 1 country.

Emmanuelle CoutanceauUnité de Génétique Moléculaire Bactérienne, Genomes and Genetics Department, Institut Pasteur, 75724 Paris, Cedex 15, France.
Jeremie Decalf
Angelo Martino
Aurélie Babon
Nathalie Winter
Stewart T Cole
Matthew L Albert
Caroline Demangel
Institut Pasteur · FR

Funding

Mycolactone-Mediated Virulence in M. ulceransR01AI049418 · NIAID · UNIVERSITY OF TENNESSEE KNOXVILLE · PI SMALL, PAMELA L. · 2001 to 2005
$1.5M
TUBERCULOSIS RESEARCH MATERIALS AND VACINE TESTINGN01AI075320 · NIAID · COLORADO STATE UNIVERSITY-FORT COLLINS · 1997 to 2004
$980k
NIAID NIH HHS N01 AI75320NIAID NIH HHS R01 AI049418NIAID NIH HHS R01 AI49418
6 · The paper itself

Abstract

Mycolactone is a polyketide toxin produced by Mycobacterium ulcerans (Mu), the causative agent of the skin disease Buruli ulcer (BU). Surprisingly, infected tissues lack inflammatory infiltrates. Structural similarities between mycolactone and immunosuppressive agents led us to investigate the immunomodulatory properties of mycolactone on dendritic cells (DCs), the key initiators and regulators of immune responses. At noncytotoxic concentrations, phenotypic and functional maturation of both mouse and human DCs was inhibited by mycolactone. Notably, mycolactone blocked the emigration of mouse-skin DCs to draining lymph nodes, as well as their maturation in vivo. In human peripheral blood-derived DCs, mycolactone inhibited the ability to activate allogeneic T cell priming and to produce inflammatory molecules. Interestingly, production of the cytokines interleukin (IL) 12, tumor necrosis factor alpha, and IL-6 was only marginally affected, whereas production of the chemokines macrophage inflammatory protein (MIP) 1alpha, MIP-1beta, regulated on activation, normal T cell expressed and secreted, interferon gamma-inducible protein 10, and monocyte chemoattractant protein 1 was abolished at nanomolar concentrations. Importantly, mycolactone endogenously expressed by Mu mediated similar inhibitory effects on beta-chemokine production by DCs. In accordance with the histopathological features of BUs, our results suggest that bacterial production of mycolactone may limit both the initiation of primary immune responses and the recruitment of inflammatory cells to the infection site. Moreover, they highlight a potential interest in mycolactone as a novel immunosuppressive agent.

Indexed as

AnimalsBacterial ToxinsCell MovementCytokinesDendritic CellsFemaleHumansImmunosuppressive AgentsLymphocyte ActivationMacrolidesMiceMice, Inbred C57BLMycobacterium ulceransBacterial ToxinsCytokinesImmunosuppressive AgentsMacrolidesmycolactone

Identifiers

PMID17517970
PMCPMC2118602
OpenAlexW2170286890

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.