Evidence map›Paper›PMID 29872095›Full record

ArticleScientific reports2018

GM-CSF targeted immunomodulation affects host response to M. tuberculosis infection.

Sulayman Benmerzoug, Fabio Vitarelli Marinho, Stéphanie Rose, Claire Mackowiak, David Gosset, Delphine Sedda, Emeline Poisson, Catherine Uyttenhove, Jacques Van Snick, Muazzam Jacobs and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

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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

13 authors at 6 institutions in 5 countries.

Sulayman BenmerzougCNRS, UMR7355, Orleans, France.
Fabio Vitarelli MarinhoCNRS, UMR7355, Orleans, France.ORCID 0000-0001-6885-3438
Stéphanie RoseCNRS, UMR7355, Orleans, France.
Claire MackowiakCNRS, UMR7355, Orleans, France.
David GossetP@CYFIC Plateform, Center for Molecular Biophysics, CNRS UPR4301, Orleans, France.
Delphine SeddaCNRS, UMR7355, Orleans, France.
Emeline PoissonCNRS, UMR7355, Orleans, France.
Catherine UyttenhoveLudwig Cancer Research, Brussels, Belgium.
Jacques Van SnickLudwig Cancer Research, Brussels, Belgium.
Muazzam JacobsDivision of Immunology, Department of Pathology and the Institute of Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
Irene GarciaDepartment of Pathology and Immunology, Centre Medical Universitaire (CMU), Faculty of Medicine, University of Geneva, Geneva, 1211, Switzerland.
Bernhard RyffelCNRS, UMR7355, Orleans, France.
Valerie F J QuesniauxCNRS, UMR7355, Orleans, France. quesniaux@cnrs-orleans.fr.ORCID 0000-0003-2907-7995
Université d'Orléans · FRLudwig Cancer Research · BECentre National de la Recherche Scientifique · FRNational Health Laboratory Service · ZAUniversidade Federal de Minas Gerais · BRUniversity of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Host directed immunomodulation represents potential new adjuvant therapies in infectious diseases such as tuberculosis. Major cytokines like TNFα exert a multifold role in host control of mycobacterial infections. GM-CSF and its receptor are over-expressed during acute M. tuberculosis infection and we asked how GM-CSF neutralization might affect host response, both in immunocompetent and in immunocompromised TNFα-deficient mice. GM-CSF neutralizing antibodies, at a dose effectively preventing acute lung inflammation, did not affect M. tuberculosis bacterial burden, but increased the number of granuloma in wild-type mice. We next assessed whether GM-CSF neutralization might affect the control of M. tuberculosis by isoniazid/rifampicin chemotherapy. GM-CSF neutralization compromised the bacterial control under sub-optimal isoniazid/rifampicin treatment in TNFα-deficient mice, leading to exacerbated lung inflammation with necrotic granulomatous structures and high numbers of intracellular M. tuberculosis bacilli. In vitro, GM-CSF neutralization promoted M2 anti-inflammatory phenotype in M. bovis BCG infected macrophages, with reduced mycobactericidal NO production and higher intracellular M. bovis BCG burden. Thus, GM-CSF pathway overexpression during acute M. tuberculosis infection contributes to an efficient M1 response, and interfering with GM-CSF pathway in the course of infection may impair the host inflammatory response against M. tuberculosis.

Indexed as

ImmunomodulationAnimalsAntibodies, NeutralizingAntitubercular AgentsCattleDisease Models, AnimalGranulocyte-Macrophage Colony-Stimulating FactorImmunologic FactorsIsoniazidMacrophagesMiceMycobacterium bovisMycobacterium tuberculosisRifampinTreatment OutcomeTuberculosis, PulmonaryAntibodies, NeutralizingAntitubercular AgentsGranulocyte-Macrophage Colony-Stimulating FactorImmunologic FactorsIsoniazidRifampin

Identifiers

PMID29872095
PMCPMC5988704
OpenAlexW2805904608

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.