Evidence map›Paper›PMID 27397585›Full record

ArticleNature communications2016

Phagocyte respiratory burst activates macrophage erythropoietin signalling to promote acute inflammation resolution.

Bangwei Luo, Jinsong Wang, Zongwei Liu, Zigang Shen, Rongchen Shi, Yu-Qi Liu, Yu Liu, Man Jiang, Yuzhang Wu, Zhiren Zhang

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 74 citations in OpenAlex.

  1. Pleiotropic effects for Parkin and LRRK2 in leprosy type-1 reactions and Parkinson's disease.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Trial
  2. Review
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  6. Microneedle Patch for In Situ Neutrophil Monitoring.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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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 1 institution in 1 country.

Bangwei LuoDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.
Jinsong WangDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.
Zongwei LiuDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.
Zigang ShenDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.
Rongchen ShiDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.
Yu-Qi LiuDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.
Yu LiuDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.
Man JiangDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.
Yuzhang WuDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.
Zhiren ZhangDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing 400038, China.ORCID 0000-0002-5238-2835
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation resolution is an active process, the failure of which causes uncontrolled inflammation which underlies many chronic diseases. Therefore, endogenous pathways that regulate inflammation resolution are fundamental and of wide interest. Here, we demonstrate that phagocyte respiratory burst-induced hypoxia activates macrophage erythropoietin signalling to promote acute inflammation resolution. This signalling is activated following acute but not chronic inflammation. Pharmacological or genetical inhibition of the respiratory burst suppresses hypoxia and macrophage erythropoietin signalling. Macrophage-specific erythropoietin receptor-deficient mice and chronic granulomatous disease (CGD) mice, which lack the capacity for respiratory burst, display impaired inflammation resolution, and exogenous erythropoietin enhances this resolution in WT and CGD mice. Mechanistically, erythropoietin increases macrophage engulfment of apoptotic neutrophils via PPARγ, promotes macrophage removal of debris and enhances macrophage migration to draining lymph nodes. Together, our results provide evidences of an endogenous pathway that regulates inflammation resolution, with important implications for treating inflammatory conditions.

Indexed as

PhagocytosisRespiratory BurstAnimalsCell MovementErythropoietinHypoxiaInflammationLymph NodesMacrophagesMaleMice, Inbred C57BLMice, KnockoutPPAR gammaReceptors, ErythropoietinSignal TransductionErythropoietinPPAR gammaReceptors, Erythropoietin

Identifiers

PMID27397585
PMCPMC4942576
OpenAlexW2460408415

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.