Evidence map›Paper›PMID 30237731›Full record

ArticleJournal of pain research2018

High glucose induces a priming effect in macrophages and exacerbates the production of pro-inflammatory cytokines after a challenge.

Rachel Grosick, Perla Abigail Alvarado-Vazquez, Amy R Messersmith, E Alfonso Romero-Sandoval

Open access · goldAbstract read
In one paragraph

Article in Journal of pain research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
  6. Review
  7. Article
  8. Advances in the Role of Stem Cell-Derived Exosomes in Diabetic Foot Wound Healing.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
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  11. Review
  12. Exendin-4 blockade of T1R2/T1R3 activation improves Pseudomonas aeruginosa-related pneumonia in an animal model of chemically induced diabetes.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Effect of Immunomodulating Extract and Some Isolates fromMolecules (Basel, Switzerland) · 2023
    Article
  18. Review
  19. Article
  20. Protective effects ofFrontiers in nutrition · 2023
    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

4 authors at 2 institutions in 1 country.

Rachel GrosickDepartment of Pharmaceutical and Administrative Science, Presbyterian College School of Pharmacy, Clinton, SC, USA.
Perla Abigail Alvarado-VazquezDepartment of Anesthesiology, Wake Forest University School Medicine, Winston-Salem, NC, USA, earomero.sandoval@gmail.com.
Amy R MessersmithDepartment of Pharmaceutical and Administrative Science, Presbyterian College School of Pharmacy, Clinton, SC, USA.
E Alfonso Romero-SandovalDepartment of Anesthesiology, Wake Forest University School Medicine, Winston-Salem, NC, USA, earomero.sandoval@gmail.com.
Presbyterian College · USWake Forest University · US

Funding

Cell-directed therapy using nanotechnology for the prevention of chronic postoperR15GM109333 · NIGMS · PRESBYTERIAN COLLEGE · PI MESSERSMITH, AMY · 2014 to 2014
$331k
NIGMS NIH HHS R15 GM109333
6 · The paper itself

Abstract

introductionPainful diabetic neuropathy is associated with chronic inflammation, in which macrophages are the key effectors. We utilized an in vitro approach to determine the effects of high glucose on macrophage phenotype. MATERIALS AND

methodsWe exposed human THP-1 macrophages to normal glucose (5 mM) and a clinically relevant high glucose environment (15 mM) and measured the expression and concentration of molecules associated with a diabetic cellular phenotype.

resultsWe found that THP-1 macrophages in high glucose conditions did not influence the basal expression of cyclooxygenase-2, Toll-like receptor-4, or class A scavenger receptor mRNA, or the concentrations of the cytokines interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, and IL-10, but induced a priming effect on tumor necrosis factor (TNF)-α. Then, we stimulated THP-1 macrophages with a strong pro-inflammatory stimulus lipopolysaccharide (LPS; 5 µg/mL). After stimulation with LPS, we observed an exacerbated increase in TNF-α, IL-6, and MCP-1 concentration in the high glucose condition compared to the normal glucose environment. THP-1 macrophages in high glucose conditions developed tolerance to IL-10 anti-inflammatory effects (TNF-α production) when challenged with LPS.

conclusionOur in vitro approach allows the study of macrophages as potential targets for therapeutic purposes since it compares them to primary human macrophages exposed to high glucose and macrophages from patients with diabetes or complications of painful diabetic neuropathy (i.e. ulcers, adipocytes, and pancreas).

Indexed as

diabeteshyperglycemiainflammationmonocyteTHP-1TNF

Identifiers

PMID30237731
PMCPMC6136416
OpenAlexW2891286842

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.