Evidence map›Paper›PMID 28851381›Full record

ArticleJournal of translational medicine2017

Glucocorticoid attenuates acute lung injury through induction of type 2 macrophage.

Guo-Wei Tu, Yi Shi, Yi-Jun Zheng, Min-Jie Ju, Hong-Yu He, Guo-Guang Ma, Guang-Wei Hao, Zhe Luo

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
3.5field-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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

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  7. Advances in anti-inflammatory treatment of sepsis-associated acute respiratory distress syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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12 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

Guo-Wei TuDepartment of Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Yi ShiBiomedical Research Center, Zhongshan Hospital, Fudan University, Shanghai, People's Republic of China.
Yi-Jun ZhengDepartment of Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Min-Jie JuDepartment of Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Hong-Yu HeDepartment of Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Guo-Guang MaDepartment of Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Guang-Wei HaoDepartment of Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Zhe LuoDepartment of Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China. luo.zhe@zs-hospital.sh.cn.ORCID 0000-0003-1384-1565
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe inflammatory lung diseases. Methylprednisolone (MP) is a common drug against inflammation in clinic. In this study, we aim to investigate the protective effect of MP on ALI and potential mechanisms.

methodsMale BABL/c mice were injected through tail vein using lipopolysaccharide (LPS, 5 mg/kg) with or without 5 mg/kg MP. Lung mechanics, tissue injury and inflammation were examined. Macrophage subsets in the lung were identified by flow cytometry. Macrophages were cultured from bone marrow of mice with or without MP. Then, we analyzed and isolated the subsets of macrophages. These isolated macrophages were then co-cultured with CD4

resultsRespiratory physiologic function was significantly improved by MP treatment. Tissue injury and inflammation were ameliorated in the MP-treated group. After MP treatment, the number of M1 decreased and M2 increased in the lung. In in vitro experiment, MP promoted M2 polarization rather than M1. We then induced M1, M2a and M2c from bone marrow cells. M1 induced more Th17 while M2 induced more CD4

conclusionIn conclusion, MP ameliorated ALI by promoting M2 polarization. M2, especially M2c, induced Tregs without any influence on Tregs immunosuppression function.

Indexed as

Acute Lung InjuryAnimalsBlood Gas AnalysisBronchoalveolar Lavage FluidCell DifferentiationChemokinesGlucocorticoidsInflammationInterleukin-10LungMacrophagesMaleMethylprednisoloneMice, Inbred BALB CModels, BiologicalOrgan SizeChemokinesGlucocorticoidsInterleukin-10MethylprednisoloneTransforming Growth Factor betaAcute lung injuryAcute respiratory distress syndromeGlucocorticoidMacrophageMethylprednisoloneRegulatory T cell

Identifiers

PMID28851381
PMCPMC5576304
OpenAlexW2752984482

What OpenQuestion holds

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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.