Evidence map›Paper›PMID 29894743›Full record

ArticleClinical immunology (Orlando, Fla.)2018

Effect of high glucose on cytokine production by human peripheral blood immune cells and type I interferon signaling in monocytes: Implications for the role of hyperglycemia in the diabetes inflammatory process and host defense against infection.

Ronghua Hu, Chang-Qing Xia, Edward Butfiloski, Michael Clare-Salzler

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

60 citing papers in PubMed, 96 citations in OpenAlex.

  1. Trial
  2. Folinic Acid Improves Healing of Diabetic Foot Ulcers.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
    Trial
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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

4 authors at 2 institutions in 2 countries.

Ronghua HuDepartment of Hematology, Xuanwu Hospital, Capital Medical University, Beijing, China; Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Chang-Qing XiaDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, USA. Electronic address: xia@pathology.ufl.edu.
Edward ButfiloskiDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Michael Clare-SalzlerDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
University of Florida · USCapital Medical University · CN

Funding

Project 3P01AI042288 · NIAID · UNIVERSITY OF FLORIDA · PI Todd Michael Brusko · 1997 to 2026
$32.9M
NIAID NIH HHS P01 AI042288
6 · The paper itself

Abstract

The major metabolic feature of diabetes is hyperglycemia which has been linked to the diabetes inflammatory processes, and diabetes-related vulnerability to infection. In the present study, we assessed how glucose affected PBMCs in type I interferon (IFN) production and subsequent signaling. We found that the moderately elevated glucose promoted, and high glucose suppressed type I IFN production, respectively. Pre-exposure to high glucose rendered monocytes more sensitive to IFN-α stimulation with heightened signaling, whereas, instantaneous addition of high glucose did not exhibit such effect. Consistent with this finding, the mRNA levels of IFN-α-induced IRF-7 in PBMCs were positively correlated with HbA1c levels of diabetes patients. Additionally, we found that high glucose promoted the production of other proinflammatory cytokines/chemokines. This study suggests that hyperglycemia may affect the inflammatory process in diabetes via promoting proinflammatory cytokines, as well as the host defense against microbial infections through impeding type I IFN production and signaling.

Indexed as

AdolescentAdultChildDiabetes ComplicationsFemaleGlucoseGlycated HemoglobinHumansHyperglycemiaImmunityInfectionsInflammationInterferon Regulatory Factor-7Interferon Type IMaleMonocytesGlucoseGlycated Hemoglobinhemoglobin A1c protein, humanInterferon Regulatory Factor-7Interferon Type ISialic Acid Binding Ig-like Lectin 1SIGLEC1 protein, humanCytokineDiabetesGlucoseHyperglycemiaInflammationInterferon

Identifiers

PMID29894743
PMCPMC6119493
OpenAlexW2805498616

What OpenQuestion holds

Textmetadata
LicenceTDM
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.