Evidence map›Paper›PMID 26690561›Full record

ArticleThe Journal of pathology2016

Low-grade inflammatory polarization of monocytes impairs wound healing.

Ruoxi Yuan, Shuo Geng, Keqiang Chen, Na Diao, Hong Wei Chu, Liwu Li

Abstract read
In one paragraph

Article in The Journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Chronic intermittent hypoxia sustains the low-grade inflammatory memory of monocytes via activation of myelopoiesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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

6 authors at 2 institutions in 1 country.

Ruoxi YuanDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA, USA.
Shuo GengDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA, USA.
Keqiang ChenDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA, USA.
Na DiaoDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA, USA.
Hong Wei ChuDepartment of Medicine, National Jewish Health, Denver, CO, USA.
Liwu LiDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA, USA.ORCID http://orcid.org/0000-0001-8870-5299
Virginia Tech · USNational Jewish Health · US

Funding

Modulation of innate immune cellular homeostasis and inflammation resolutionR01HL115835 · NHLBI · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI LI, LIWU · 2012 to 2021
$3.6M
IRAK-M in lung defense against rhinovirus infectionR01AI106287 · NIAID · NATIONAL JEWISH HEALTH · PI CHU, HONG W, LI, LIWU · 2014 to 2018
$2.0M
The novel role and regulation of IRAK in innate immunityR01AI064414 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LI, LIWU · 2005 to 2010
$1.9M
Regulation of signaling events in septic leukocytesR01AI050089 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LI, LIWU · 2002 to 2006
$1.5M
Novel Innate Receptor for the Fungal PAMP chitinR21AI115986 · NIAID · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI LAWRENCE, CHRISTOPHER BRIAN, LI, LIWU · 2015 to 2016
$427k
Innate priming in sepsis exacerbationR56AI108264 · NIAID · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI LI, LIWU · 2014 to 2014
$403k
NHLBI NIH HHS R01 HL115835NIAID NIH HHS R01 AI050089NIAID NIH HHS R01 AI064414NIAID NIH HHS R01 AI106287NIAID NIH HHS R01AI115986NIAID NIH HHS R21 AI115986NIAID NIH HHS R56 AI108264NIAID NIH HHS R56AI108264
6 · The paper itself

Abstract

Impaired wound healing often accompanies low-grade inflammatory conditions, during which circulating levels of subclinical super-low-dose endotoxin may persist. Low-grade inflammatory monocyte polarization may occur during chronic inflammation and deter effective wound repair. However, little is understood about the potential mechanisms of monocyte polarization by sustained insult of subclinical super-low-dose endotoxin. We observed that super-low-dose endotoxin preferentially programmes a low-grade inflammatory monocyte state in vitro and in vivo, as represented by the elevated population of CD11b(+) Ly6C(high) monocytes and sustained expression of CCR5. Mechanistically, super-low-dose endotoxin caused cellular stress, altered lysosome function and increased the transcription factor IRF5. TUDCA, a potent inhibitor of cellular stress, effectively blocked monocyte polarization and improved wound healing in mice injected with super-low-dose endotoxin. Our data revealed the polarization of low-grade inflammatory monocytes by sustained endotoxin challenge, its underlying mechanisms and a potential intervention strategy. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Indexed as

Cell PolarityHumansInflammationLysosomesMacrophagesMonocytesTranscription FactorsWound HealingTranscription Factorscellular stressinnate immunityIRF5low-grade inflammationmonocyteswound healing

Identifiers

PMID26690561
PMCPMC4760849
OpenAlexW2212380157

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.