Evidence map›Paper›PMID 34517005›Full record

ArticleThe Journal of investigative dermatology2022

IL-10 Dysregulation Underlies Chemokine Insufficiency, Delayed Macrophage Response, and Impaired Healing in Diabetic Wounds.

Ruchi Roy, Janet Zayas, Mohamed F Mohamed, Anahita Aboonabi, Kaylee Delgado, Jennillee Wallace, Mohammad Bayat, Timothy M Kuzel, Jochen Reiser, Sasha H Shafikhani

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  7. Frontiers in microbiology · 2026
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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

10 authors at 2 institutions in 2 countries.

Ruchi RoyDepartment of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA; Division of Hematology, Oncology and Cell Therapy, Rush University Medical Center, Chicago, Illinois, USA.
Janet ZayasDepartment of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA; Division of Hematology, Oncology and Cell Therapy, Rush University Medical Center, Chicago, Illinois, USA; Department of Microbial Pathogens and Immunity, Rush University Medical Center, Chicago, Illinois, USA.
Mohamed F MohamedDepartment of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA; Division of Hematology, Oncology and Cell Therapy, Rush University Medical Center, Chicago, Illinois, USA.
Anahita AboonabiDepartment of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA; Division of Hematology, Oncology and Cell Therapy, Rush University Medical Center, Chicago, Illinois, USA.
Kaylee DelgadoDepartment of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA; Division of Hematology, Oncology and Cell Therapy, Rush University Medical Center, Chicago, Illinois, USA.
Jennillee WallaceDepartment of Microbial Pathogens and Immunity, Rush University Medical Center, Chicago, Illinois, USA.
Mohammad BayatDepartment of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Price Institute of Surgical Research, University of Louisville and Noveratech LLC. of Louisville, Louisville, Kentucky, USA.
Timothy M KuzelDepartment of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA; Division of Hematology, Oncology and Cell Therapy, Rush University Medical Center, Chicago, Illinois, USA.
Jochen ReiserDepartment of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA.
Sasha H ShafikhaniDepartment of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA; Division of Hematology, Oncology and Cell Therapy, Rush University Medical Center, Chicago, Illinois, USA; Department of Microbial Pathogens and Immunity, Rush University Medical Center, Chicago, Illinois, USA; Cancer Center, Rush University Medical Center, Chicago, Illinois, USA. Electronic address: Sasha_Shafikhani@rush.edu.
Rush University Medical Center · USUniversity of Louisville · US

Funding

Role of immune system in prophylaxis antibiotic's surgical site infection controlR01AI150668 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI SHAFIKHANI, SASHA H · 2020 to 2024
$2.0M
Factors Leading to Enhanced Pseudomonas Aeruginosa Infection in Diabetic WoundsR01DK107713 · NIDDK · RUSH UNIVERSITY MEDICAL CENTER · PI SHAFIKHANI, SASHA H · 2016 to 2020
$1.7M
Factors Leading to Enhanced Bacterial Infection in Diabetic WoundsF31DK118797 · NIDDK · RUSH UNIVERSITY MEDICAL CENTER · PI ZAYAS, JANET PATRICIA · 2018 to 2019
$90k
NIAID NIH HHS R01 AI150668NIDDK NIH HHS F31 DK118797NIDDK NIH HHS R01 DK107713
6 · The paper itself

Abstract

Persistent inflammation is a major contributor to healing impairment in diabetic chronic wounds. Paradoxically, diabetic wound environment during the acute phase of healing is completely different because it exhibits a reduced macrophage response owing to inadequate expression of CCL2 proinflammatory cytokine. What causes a reduction in CCL2 expression in diabetic wounds early after injury remains unknown. In this study, we report that in contrast to prolonged exposure to high glucose, which makes monocytes proinflammatory, short-term exposure to high glucose causes a rapid monocyte reprogramming, manifested by increased expression and secretion of IL-10, which in an autocrine/paracrine fashion reduces glucose uptake and transforms monocytes into an anti-inflammatory phenotype by dampening signaling through toll-like receptors. We show that IL-10 expression is significantly increased in diabetic wounds during the acute phase of healing, causing significant reductions in toll-like receptor signaling and proinflammatory cytokine production, delaying macrophage and leukocyte responses, and underlying healing impairment in diabetic wounds. Importantly, blocking IL-10 signaling during the acute phase of healing improves toll-like receptor signaling, increases proinflammatory cytokine production, enhances macrophage and leukocyte responses, and stimulates healing in diabetic wounds. We posit that anti-IL-10 strategies have therapeutic potential if added topically after surgical debridement, which resets chronic wounds into acute fresh wounds.

Indexed as

Diabetes MellitusInterleukin-10ChemokinesGlucoseHumansMacrophagesChemokinesGlucoseIL10 protein, humanInterleukin-10

Identifiers

PMID34517005
PMCPMC8860852
OpenAlexW3199890004

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.