Evidence map›Paper›PMID 28422970›Full record

ArticlePLoS neglected tropical diseases2017

The gut microbiota as a modulator of innate immunity during melioidosis.

Jacqueline M Lankelma, Emma Birnie, Tassili A F Weehuizen, Brendon P Scicluna, Clara Belzer, Riekelt H Houtkooper, Joris J T H Roelofs, Alex F de Vos, Tom van der Poll, Andries E Budding and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.1field-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

35 citing papers in PubMed, 52 citations in OpenAlex.

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  20. Gut Microbiota Contributes to Host Defense AgainstJournal of inflammation research · 2021
    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

11 authors at 4 institutions in 1 country.

Jacqueline M LankelmaCenter for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Emma BirnieCenter for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Tassili A F WeehuizenCenter for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Brendon P SciclunaCenter for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Clara BelzerLaboratory of Microbiology, Wageningen University, Wageningen, The Netherlands.
Riekelt H HoutkooperLaboratory Genetic Metabolic Diseases, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Joris J T H RoelofsDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Alex F de VosCenter for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Tom van der PollCenter for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Andries E BuddingDepartment of Medical Microbiology, Vrije Universiteit, Amsterdam, The Netherlands.
W Joost WiersingaCenter for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
University of Amsterdam · NLAcademic Medical Center · NLVrije Universiteit Amsterdam · NLWageningen University & Research · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMelioidosis, caused by the Gram-negative bacterium Burkholderia pseudomallei, is an emerging cause of pneumonia-derived sepsis in the tropics. The gut microbiota supports local mucosal immunity and is increasingly recognized as a protective mediator in host defenses against systemic infection. Here, we aimed to characterize the composition and function of the intestinal microbiota during experimental melioidosis. METHODOLOGY/PRINCIPAL

findingsC57BL/6 mice were infected intranasally with B. pseudomallei and sacrificed at different time points to assess bacterial loads and inflammation. In selected experiments, the gut microbiota was disrupted with broad-spectrum antibiotics prior to inoculation. Fecal bacterial composition was analyzed by means of IS-pro, a 16S-23S interspacer region-based profiling method. A marked shift in fecal bacterial composition was seen in all mice during systemic B. pseudomallei infection with a strong increase in Proteobacteria and decrease in Actinobacteria, with an increase in bacterial diversity. We found enhanced early dissemination of B. pseudomallei and systemic inflammation during experimental melioidosis in microbiota-disrupted mice compared with controls. Whole-genome transcriptional profiling of the lung identified several genes that were differentially expressed between mice with a normal or disrupted intestinal microbiota. Genes involved in acute phase signaling, including macrophage-related signaling pathways were significantly elevated in microbiota disrupted mice. Compared with controls, alveolar macrophages derived from antibiotic pretreated mice showed a diminished capacity to phagocytose B. pseudomallei. This might in part explain the observed protective effect of the gut microbiota in the host defense against pneumonia-derived melioidosis. CONCLUSIONS/SIGNIFICANCE: Taken together, these data identify the gut microbiota as a potential modulator of innate immunity during B. pseudomallei infection.

Indexed as

Immunity, InnateAnimalsAnti-Bacterial AgentsBacteriaDisease Models, AnimalDNA, Ribosomal SpacerGastrointestinal MicrobiomeGastrointestinal TractGene Expression ProfilingImmunologic FactorsLungMelioidosisMice, Inbred C57BLAnti-Bacterial AgentsDNA, Ribosomal SpacerImmunologic Factors

Identifiers

PMID28422970
PMCPMC5411098
OpenAlexW2605952725

What OpenQuestion holds

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LicenceCC BY
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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.