Evidence map›Paper›PMID 32030817›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Resident alveolar macrophage-derived vesicular SOCS3 dampens allergic airway inflammation.

Christina Draijer, Jennifer M Speth, Loka R K Penke, Zbigniew Zaslona, Joseph D Bazzill, Njira Lugogo, Yvonne J Huang, James J Moon, Marc Peters-Golden

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 51 citations in OpenAlex.

  1. The role of myeloid immune cells in lung epithelial repair.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
  2. Review
  3. Alveolar macrophage-neutrophil crosstalk in acute lung injury: mechanisms, feedback loops, and therapeutic opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  4. Review
  5. Article
  6. 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
    Review
  7. Article
  8. Article
  9. Harmonising cellular conversations: decoding the vital roles of extracellular vesicles in respiratory system intercellular communications.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  10. Cell-cell communication: new insights and clinical implications.Signal transduction and targeted therapy · 2024
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Interaction between alveolar macrophages and epithelial cells duringFrontiers in cellular and infection microbiology · 2023
    Review
  18. IFN-American journal of respiratory cell and molecular biology · 2023
    Article
  19. Review
  20. Review
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

9 authors at 1 institution in 1 country.

Christina DraijerDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Jennifer M SpethDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Loka R K PenkeDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Zbigniew ZaslonaDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Joseph D BazzillDepartment of Pharmaceutical Sciences, University of Michigan, Ann Arbor, MI, USA.
Njira LugogoDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Yvonne J HuangDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
James J MoonDepartment of Pharmaceutical Sciences, University of Michigan, Ann Arbor, MI, USA.
Marc Peters-GoldenDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · US

Funding

PULMONARY CELLULAR AND MOLECULAR BIOLOGY TRAININGT32HL007749 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Pickett Dickson · 1993 to 2026
$19.9M
Novel Functions of Lung Macrophages and Fibroblasts in Pulmonary Inflammation and FibrosisR35HL144979 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2019 to 2025
$6.5M
Sputum Microbial Markers of Type 2-Low AsthmaR01AI129958 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HUANG, YVONNE JEAN · 2017 to 2021
$3.6M
Secreted SOCS Proteins as Vectors of Lung Macrophage to Epithelial Cell CrosstalkR01HL125555 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2015 to 2018
$2.2M
NHLBI NIH HHS R01 HL125555NHLBI NIH HHS R35 HL144979NHLBI NIH HHS T32 HL007749NIAID NIH HHS R01 AI129958
6 · The paper itself

Abstract

Resident alveolar macrophages (AMs) suppress allergic inflammation in murine asthma models. Previously we reported that resident AMs can blunt inflammatory signaling in alveolar epithelial cells (ECs) by transcellular delivery of suppressor of cytokine signaling 3 (SOCS3) within extracellular vesicles (EVs). Here we examined the role of vesicular SOCS3 secretion as a mechanism by which AMs restrain allergic inflammatory responses in airway ECs. Bronchoalveolar lavage fluid (BALF) levels of SOCS3 were reduced in asthmatics and in allergen-challenged mice. Ex vivo SOCS3 secretion was reduced in AMs from challenged mice and this defect was mimicked by exposing normal AMs to cytokines associated with allergic inflammation. Both AM-derived EVs and synthetic SOCS3 liposomes inhibited the activation of STAT3 and STAT6 as well as cytokine gene expression in ECs challenged with IL-4/IL-13 and house dust mite (HDM) extract. This suppressive effect of EVs was lost when they were obtained from AMs exposed to allergic inflammation-associated cytokines. Finally, inflammatory cell recruitment and cytokine generation in the lungs of OVA-challenged mice were attenuated by intrapulmonary pretreatment with SOCS3 liposomes. Overall, AM secretion of SOCS3 within EVs serves as a brake on airway EC responses during allergic inflammation, but is impaired in asthma. Synthetic liposomes encapsulating SOCS3 can rescue this defect and may serve as a framework for novel therapeutic approaches targeting airway inflammation.

Indexed as

AdolescentAdultAgedAnimalsAsthmaBlotting, WesternCell LineCell PolarityFemaleHumansHypersensitivityInflammationInterleukin-33Interleukin-4LiposomesMacrophagesIL33 protein, humanInterleukin-33Interleukin-4LiposomesSuppressor of Cytokine Signaling 3 Proteinallergic airway inflammationalveolar macrophagesepithelial cellsextracellular vesiclesliposomessuppressor of cytokine signaling 3

Identifiers

PMID32030817
PMCPMC7433762
OpenAlexW3004553547

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.