Evidence map›Paper›PMID 27834919›Full record

ArticleInternational journal of molecular sciences2016

Increased Expression Profile and Functionality of TLR6 in Peripheral Blood Mononuclear Cells and Hepatocytes of Morbidly Obese Patients with Non-Alcoholic Fatty Liver Disease.

María Teresa Arias-Loste, Paula Iruzubieta, Ángela Puente, David Ramos, Carolina Santa Cruz, Ángel Estébanez, Susana Llerena, Carmen Alonso-Martín, David San Segundo, Lorena Álvarez and 4 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2016. 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 12% 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, 36 citations in OpenAlex.

  1. Review
  2. The Role of TLRs in Obesity and Its Related Metabolic Disorders.International journal of molecular sciences · 2025
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  15. The Exercise Training Modulatory Effects on the Obesity-Induced Immunometabolic Dysfunctions.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Review
  16. Innate immune regulatory networks in hepatic lipid metabolism.Journal of molecular medicine (Berlin, Germany) · 2019
    Review
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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

14 authors at 2 institutions in 1 country.

María Teresa Arias-LosteGastroenterology and Hepatology Department, Marqués de Valdecilla University Hospital, 39008 Santander, Spain. ariasloste@gmail.com.
Paula IruzubietaGastroenterology and Hepatology Department, Marqués de Valdecilla University Hospital, 39008 Santander, Spain. piruzubieta@gmail.com.
Ángela PuenteGastroenterology and Hepatology Department, Marqués de Valdecilla University Hospital, 39008 Santander, Spain. anpuente@humv.es.
David RamosInfection, Immunity and Digestive Pathology Group, Research Institute Marqués de Valdecilla (IDIVAL), 390008 Santander, Spain. david.ramos.m@gmail.com.
Carolina Santa CruzTransplant and Autoimmunity Group, Research Institute Marqués de Valdecilla (IDIVAL), 39008 Santander, Spain. loraksc@gmail.com.
Ángel EstébanezInfection, Immunity and Digestive Pathology Group, Research Institute Marqués de Valdecilla (IDIVAL), 390008 Santander, Spain. aesga@hotmail.com.
Susana LlerenaGastroenterology and Hepatology Department, Marqués de Valdecilla University Hospital, 39008 Santander, Spain. susanallerena@hotmail.com.
Carmen Alonso-MartínGastroenterology and Hepatology Department, Marqués de Valdecilla University Hospital, 39008 Santander, Spain. maika_1387@hotmail.com.
David San SegundoTransplant and Autoimmunity Group, Research Institute Marqués de Valdecilla (IDIVAL), 39008 Santander, Spain. david_san_segundo@hotmail.com.
Lorena ÁlvarezTransplant and Autoimmunity Group, Research Institute Marqués de Valdecilla (IDIVAL), 39008 Santander, Spain. lorenalvar@hotmail.com.
Antonio López UserosGeneral Surgery Department, Marqués de Valdecilla University Hospital, 39008 Santander, Spain. alopez@humv.es.
Emilio FábregaGastroenterology and Hepatology Department, Marqués de Valdecilla University Hospital, 39008 Santander, Spain. digfge@humv.es.
Marcos López-HoyosTransplant and Autoimmunity Group, Research Institute Marqués de Valdecilla (IDIVAL), 39008 Santander, Spain. mlopezhoyos@humv.es.
Javier CrespoGastroenterology and Hepatology Department, Marqués de Valdecilla University Hospital, 39008 Santander, Spain. javiercrespo1991@gmail.com.
Marqués de Valdecilla University Hospital · ESInstituto de Investigación Marqués de Valdecilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current evidence suggests that gut dysbiosis drives obesity and non-alcoholic fatty liver disease (NAFLD) pathogenesis. Toll-like receptor 2 (TLR2) and TLR6 specifically recognize components of Gram-positive bacteria. Despite the potential implications of TLR2 in NAFLD pathogenesis, the role of TLR6 has not been addressed. Our aim is to study a potential role of TLR6 in obesity-related NAFLD. Forty morbidly obese patients undergoing bariatric surgery were prospectively studied. Cell surface expression of TLR2 and TLR6 was assessed on peripheral blood mononuclear cells (PBMCs) by flow cytometry. Freshly isolated monocytes were cultured with specific TLR2/TLR6 agonists and intracellular production of cytokines was determined by flow-cytometry. In liver biopsies, the expression of TLR2 and TLR6 was analyzed by immunohistochemistry and cytokine gene expression using RT-qPCR. TLR6 expression in PBMCs from non-alcoholic steatohepatitis (NASH) patients was significantly higher when compared to those from simple steatosis. The production of pro-inflammatory cytokines in response to TLR2/TLR6 stimulation was also significantly higher in patients with lobular inflammation. Hepatocyte expression of TLR6 but not that of TLR2 was increased in NAFLD patients compared to normal liver histology. Deregulated expression and activity of peripheral TLR6 in morbidly obese patients can mirror the liver inflammatory events that are well known drivers of obesity-related NASH pathogenesis. Moreover, TLR6 is also significantly overexpressed in the hepatocytes of NAFLD patients compared to their normal counterparts. Thus, deregulated TLR6 expression may potentiate TLR2-mediated liver inflammation in NAFLD pathogenesis, and also serve as a potential peripheral biomarker of obesity-related NASH.

Indexed as

AdultCells, CulturedCytokinesFemaleFlow CytometryGene ExpressionHepatocytesHumansImmunohistochemistryLeukocytes, MononuclearMaleMiddle AgedNon-alcoholic Fatty Liver DiseaseObesity, MorbidProspective StudiesReverse Transcriptase Polymerase Chain ReactionCytokinesTLR2 protein, humanTLR6 protein, humanToll-Like Receptor 2Toll-Like Receptor 6lobular inflammationmorbid obesitynon-alcoholic fatty liver diseasepro-inflammatory cytokinesTLR2TLR6

Identifiers

PMID27834919
PMCPMC5133878
OpenAlexW2550430758

What OpenQuestion holds

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Registered trials

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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.