Evidence map›Paper›PMID 25309919›Full record

ArticleBioMed research international2014

Cervical cancer cell supernatants induce a phenotypic switch from U937-derived macrophage-activated M1 state into M2-like suppressor phenotype with change in Toll-like receptor profile.

Karina Sánchez-Reyes, Alejandro Bravo-Cuellar, Georgina Hernández-Flores, José Manuel Lerma-Díaz, Luis Felipe Jave-Suárez, Paulina Gómez-Lomelí, Ruth de Celis, Adriana Aguilar-Lemarroy, Jorge Ramiro Domínguez-Rodríguez, Pablo Cesar Ortiz-Lazareno

Abstract 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

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  13. Correlation of Circulating CD64Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2017
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  18. A clinicopathological study of episomal papillomavirus infection of the human placenta and pregnancy complications.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2015
    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

10 authors.

Karina Sánchez-ReyesDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico ; Programa de Doctorado en Ciencias Biomédicas Orientación Inmunología, Centro Universitario de Ciencias de la Salud (CUCS), Universidad de Guadalajara, 44340 Guadalajara, JAL, Mexico.
Alejandro Bravo-CuellarDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico ; Departamento de Ciencias de la Salud, Centro Universitario de los Altos, Universidad de Guadalajara, Tepatitlán de Morelos, 47600 Guadalajara, JAL, Mexico.
Georgina Hernández-FloresDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico.
José Manuel Lerma-DíazDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico ; Departamento de Ciencias de la Salud, Centro Universitario de los Altos, Universidad de Guadalajara, Tepatitlán de Morelos, 47600 Guadalajara, JAL, Mexico.
Luis Felipe Jave-SuárezDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico.
Paulina Gómez-LomelíDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico ; Programa de Doctorado en Ciencias Biomédicas Orientación Inmunología, Centro Universitario de Ciencias de la Salud (CUCS), Universidad de Guadalajara, 44340 Guadalajara, JAL, Mexico.
Ruth de CelisDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico.
Adriana Aguilar-LemarroyDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico.
Jorge Ramiro Domínguez-RodríguezDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico ; Departamento de Farmacobiología, Centro Universitario de Ciencias Exactas e Ingeniería, Universidad de Guadalajara, 44430 Guadalajara, JAL, Mexico.
Pablo Cesar Ortiz-LazarenoDivisión de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, 44340 Guadalajara, JAL, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledCervical cancer (CC) is the second most common cancer among women worldwide. Infection with human papillomavirus (HPV) is the main risk factor for developing CC. Macrophages are important immune effector cells; they can be differentiated into two phenotypes, identified as M1 (classically activated) and M2 (alternatively activated). Macrophage polarization exerts profound effects on the Toll-like receptor (TLR) profile. In this study, we evaluated whether the supernatant of human CC cells HeLa, SiHa, and C-33A induces a shift of M1 macrophage toward M2 macrophage in U937-derived macrophages.

resultsThe results showed that soluble factors secreted by CC cells induce a change in the immunophenotype of macrophages from macrophage M1 into macrophage M2. U937-derived macrophages M1 released proinflammatory cytokines and nitric oxide; however, when these cells were treated with the supernatant of CC cell lines, we observed a turnover of M1 toward M2. These cells increased CD163 and IL-10 expression. The expression of TLR-3, -7, and -9 is increased when the macrophages were treated with the supernatant of CC cells.

conclusionsOur result strongly suggests that CC cells may, through the secretion of soluble factors, induce a change of immunophenotype M1 into M2 macrophages.

Indexed as

Macrophage ActivationAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCell Line, TumorCytokinesFemaleHumansInflammation MediatorsLipopolysaccharidesNitric OxidePhenotypeReceptors, Cell SurfaceSubcellular FractionsToll-Like Receptor 3Toll-Like Receptor 7Antigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCytokinesInflammation MediatorsLipopolysaccharidesNitric OxideReceptors, Cell SurfaceToll-Like Receptor 3Toll-Like Receptor 7Toll-Like Receptor 9Toll-Like Receptors

Identifiers

PMID25309919
PMCPMC4189768

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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.