Evidence map›Paper›PMID 22732594›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Critical role for CCAAT/enhancer-binding protein β in immune complex-induced acute lung injury.

Chunguang Yan, Min Wu, Jay Cao, Huifang Tang, Mei Zhu, Peter F Johnson, Hongwei Gao

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Sex differences in the expression of lung inflammatory mediators in response to ozone.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. LPS-treated macrophage cytokines repress surfactant protein-B in lung epithelial cells.American journal of respiratory cell and molecular biology · 2013
    Article
  19. Article
  20. The many faces of C/EBPδ and their relevance for inflammation and cancer.International journal of biological sciences · 2013
    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

7 authors at 5 institutions in 1 country.

Chunguang YanDepartment of Anesthesiology, Perioperative, and Pain Medicine, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Min Wu
Jay Cao
Huifang Tang
Mei Zhu
Peter F Johnson
Hongwei Gao
Brigham and Women's Hospital · USHarvard University · USAgricultural Research Service · USNational Cancer Institute · USUniversity of North Dakota · US

Funding

Role of CEBP transcription factors in regulating cell growth and tumorigenesisZIABC010328 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI JOHNSON, PETER F · 2009 to 2021
$17.5M
STAT3 and its Acetylation in Acute Lung InjuryR01HL092905 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GAO, HONGWEI · 2008 to 2012
$1.8M
DNA Based Repair and MAP kinasesR03ES014690 · NIEHS · UNIVERSITY OF NORTH DAKOTA · PI WU, MIN · 2006 to 2007
$138k
Intramural NIH HHSNHLBI NIH HHS 3R01HL092905-02S1NHLBI NIH HHS 5R01HL092905-04NHLBI NIH HHS R01 HL092905NIEHS NIH HHS ES014690NIEHS NIH HHS R03 ES014690
6 · The paper itself

Abstract

C/EBPs, particularly C/EBPβ and C/EBPδ, are known to participate in the regulation of many genes associated with inflammation. However, very little is known regarding the activation and functions of C/EBPβ and C/EBPδ in acute lung inflammation and injury. In this study, we show that both C/EBPβ and C/EBPδ activation are triggered in lungs and in alveolar macrophages following intrapulmonary deposition of IgG immune complexes. We further show that mice carrying a targeted deletion of the C/EBPβ gene displayed significant attenuation of the permeability index (lung vascular leak of albumin), lung neutrophil accumulation (myeloperoxidase activity), total number of WBCs, and neutrophils in bronchoalveolar lavage fluids compared with wild-type mice. Moreover, the mutant mice expressed considerably less TNF-α, IL-6, and CXC/CC chemokine and soluble ICAM-1 proteins in bronchoalveolar lavage fluids, and corresponding mRNAs in the IgG immune complex-injured lung, compared with wild-type mice. These phenotypes were associated with a significant reduction in morphological lung injury. In contrast, C/EBPδ deficiency had no effect on IgG immune complex-induced lung injury. IgG immune complex-stimulated C/EBPβ-deficient alveolar macrophages released significantly less TNF-α, IL-6, MIP-2, keratinocyte cell-derived chemokine, and MIP-1α compared with wild-type cells. Similar decreases in IgG immune complex-induced inflammatory mediator production were observed following small interfering RNA ablation of C/EBPβ in a murine alveolar macrophage cell line. These findings implicate C/EBPβ as a critical regulator of IgG immune complex-induced inflammatory responses and injury in the lung.

Indexed as

Acute Lung InjuryAnimalsAntigen-Antibody ComplexCCAAT-Enhancer-Binding Protein-betaCCAAT-Enhancer-Binding Protein-deltaCell LineDisease Models, AnimalImmunoglobulin GInflammation MediatorsMacrophages, AlveolarMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutAntigen-Antibody ComplexCCAAT-Enhancer-Binding Protein-betaCCAAT-Enhancer-Binding Protein-deltaCebpd protein, mouseImmunoglobulin GInflammation Mediators

Identifiers

PMID22732594
PMCPMC3401325
OpenAlexW2142268747

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.