Evidence map›Paper›PMID 24949482›Full record

ArticleBioMed research international2014

Differential macrophage response to slow- and fast-growing pathogenic mycobacteria.

A Cecilia Helguera-Repetto, Rommel Chacon-Salinas, Jorge F Cerna-Cortes, Sandra Rivera-Gutierrez, Vianney Ortiz-Navarrete, Iris Estrada-Garcia, Jorge A Gonzalez-y-Merchand

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 32 citations in OpenAlex.

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  16. Frontiers in microbiology · 2018
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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

7 authors at 2 institutions in 1 country.

A Cecilia Helguera-RepettoDepartamento de Microbiologia, Escuela Nacional de Ciencias Biologicas (ENCB), Instituto Politecnico Nacional (IPN), 11340 México City, DF, Mexico ; Departamento de Inmunobioquímica, Torre de Investigación, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes (INPer), Montes Urales 800, Colonia Lomas de Virreyes, 11000 México City, DF, Mexico.
Rommel Chacon-SalinasDepartamento de Inmunologia, Escuela Nacional de Ciencias Biologicas, Instituto Politecnico Nacional (IPN), 11340 México City, DF, Mexico.
Jorge F Cerna-CortesDepartamento de Microbiologia, Escuela Nacional de Ciencias Biologicas (ENCB), Instituto Politecnico Nacional (IPN), 11340 México City, DF, Mexico.
Sandra Rivera-GutierrezDepartamento de Microbiologia, Escuela Nacional de Ciencias Biologicas (ENCB), Instituto Politecnico Nacional (IPN), 11340 México City, DF, Mexico.
Vianney Ortiz-NavarreteDepartamento of Biomedicina Molecular, Centro de Investigacion y de Estudios Avanzados (CINVESTAV), IPN, 07360 México City, DF, Mexico.
Iris Estrada-GarciaDepartamento de Inmunologia, Escuela Nacional de Ciencias Biologicas, Instituto Politecnico Nacional (IPN), 11340 México City, DF, Mexico.
Jorge A Gonzalez-y-MerchandDepartamento de Microbiologia, Escuela Nacional de Ciencias Biologicas (ENCB), Instituto Politecnico Nacional (IPN), 11340 México City, DF, Mexico.
Instituto Politécnico Nacional · MXCenter for Research and Advanced Studies of the National Polytechnic Institute · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nontuberculous mycobacteria (NTM) have recently been recognized as important species that cause disease even in immunocompetent individuals. The mechanisms that these species use to infect and persist inside macrophages are not well characterised. To gain insight concerning this process we used THP-1 macrophages infected with M. abscessus, M. fortuitum, M. celatum, and M. tuberculosis. Our results showed that slow-growing mycobacteria gained entrance into these cells with more efficiency than fast-growing mycobacteria. We have also demonstrated that viable slow-growing M. celatum persisted inside macrophages without causing cell damage and without inducing reactive oxygen species (ROS), as M. tuberculosis caused. In contrast, fast-growing mycobacteria destroyed the cells and induced high levels of ROS. Additionally, the macrophage cytokine pattern induced by M. celatum was different from the one induced by either M. tuberculosis or fast-growing mycobacteria. Our results also suggest that, in some cases, the intracellular survival of mycobacteria and the immune response that they induce in macrophages could be related to their growth rate. In addition, the modulation of macrophage cytokine production, caused by M. celatum, might be a novel immune-evasion strategy used to survive inside macrophages that is different from the one reported for M. tuberculosis.

Indexed as

Immunity, CellularCytokinesHumansMacrophagesMycobacterium Infections, NontuberculousNontuberculous MycobacteriaReactive Oxygen SpeciesCytokinesReactive Oxygen Species

Identifiers

PMID24949482
PMCPMC4052160
OpenAlexW2166909448

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.