Evidence map›Paper›PMID 25420919›Full record

ArticleJournal of leukocyte biology2015

Distinct role of FoxO1 in M-CSF- and GM-CSF-differentiated macrophages contributes LPS-mediated IL-10: implication in hyperglycemia.

Sangwoon Chung, Ravi Ranjan, Yong Gyu Lee, Gye Young Park, Manjula Karpurapu, Jing Deng, Lei Xiao, Ji Young Kim, Terry G Unterman, John W Christman

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.0field-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

53 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Research progress on the mechanism of FOXO protein in sepsis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. FoxO1 promotes high glucose-induced inflammation and cataract formation via JAK1/STAT1.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025
    Article
  4. Review
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  18. Article
  19. Interleukin 26 Induces Macrophage IL-9 Expression in Rheumatoid Arthritis.International journal of molecular sciences · 2023
    Article
  20. Article
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 3 institutions in 1 country.

Sangwoon Chung*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA.
Ravi Ranjan*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA.
Yong Gyu Lee*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA.
Gye Young Park*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA.
Manjula Karpurapu*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA.
Jing Deng*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA.
Lei Xiao*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA.
Ji Young Kim*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA.
Terry G Unterman*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA.
John W Christman*Division of Pulmonary, Allergy, Critical Care, and Sleep, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA; Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Illinois, USA; and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA John.Christman@osumc.edu.
The Ohio State University · USUniversity of Illinois Chicago · USJesse Brown VA Medical Center · US

Funding

Macrophage Gene Expression in Acute Lung InflammationR01HL075557 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHRISTMAN, JOHN W · 2004 to 2016
$4.8M
NADPH OXIDASE REGULATION OF THE MACROPHAGE INFLAMMATORY PHENOTYPE IN SEPSISR01HL103643 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHRISTMAN, JOHN W · 2010 to 2013
$1.5M
Regulation of Neutrophilic Lung InflammationI01BX000108 · VA · JESSE BROWN VA MEDICAL CENTER · PI CHRISTMAN, JOHN W · 2009 to 2013
–
Regulation of Hepatic Gene Expression and Metabolism by FoxO ProteinsI01BX001968 · VA · JESSE BROWN VA MEDICAL CENTER · PI UNTERMAN, TERRY G. · 2013 to 2023
–
BLRD VA I01 BX000108BLRD VA I01 BX001968NHLBI NIH HHS 2R01HL075557-08NHLBI NIH HHS 5R01HL103643-03NHLBI NIH HHS R01 HL075557NHLBI NIH HHS R01 HL103643
6 · The paper itself

Abstract

Macrophages are a heterogeneous population of immune cells that are essential for the initiation and containment inflammation. There are 2 well-established populations of inflammatory macrophages: classically activated M1 and alternatively activated M2 macrophages. The FoxO family of transcription factors plays key roles in a number of cellular processes, including cell growth, metabolism, survival, and inflammation. In this study, we determined whether the expression of FoxO1 contributes polarization of macrophages toward the M2-like phenotype by enhancing IL-10 cytokine expression. We identified that FoxO1 is highly expressed in M-CSF-derived (M2-like) macrophage subsets, and this M2-like macrophages showed a preferential FoxO1 enrichment on the IL-10 promoter but not in GM-CSF-derived (M1-like) macrophages during classic activation by LPS treatment, which suggests that FoxO1 enhances IL-10 by binding directly to the IL-10 promoter, especially in BMMs. In addition, our data show that macrophages in the setting of hyperglycemia contribute to the macrophage-inflammatory phenotype through attenuation of the contribution of FoxO1 to activate IL-10 expression. Our data identify a novel role for FoxO1 in regulating IL-10 secretion during classic activation and highlight the potential for therapeutic interventions for chronic inflammatory conditions, such as atherosclerosis, diabetes, inflammatory bowel disease, and arthritis.

Indexed as

AnimalsCell DifferentiationCell LineFemaleForkhead Box Protein O1Forkhead Transcription FactorsGranulocyte-Macrophage Colony-Stimulating FactorHumansHyperglycemiaInterleukin-10LipopolysaccharidesMacrophage ActivationMacrophage Colony-Stimulating FactorMacrophagesMaleMiceForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanFoxo1 protein, mouseGranulocyte-Macrophage Colony-Stimulating FactorIL10 protein, humanIL10 protein, mouseInterleukin-10LipopolysaccharidesMacrophage Colony-Stimulating FactorinflammationM1-likeM2-likemetabolic stressmonocyte

Identifiers

PMID25420919
PMCPMC4304426
OpenAlexW1968153747

What OpenQuestion holds

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Registered trials

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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.