Evidence map›Paper›PMID 25005359›Full record

ArticleMucosal immunology2015

Matrix protein CCN1 induced by bacterial DNA and CpG ODN limits lung inflammation and contributes to innate immune homeostasis.

H-G Moon, Z Qin, T Quan, L Xie, C S Dela Cruz, Y Jin

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

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The Roles of CCN1/CYR61 in Pulmonary Diseases.International journal of molecular sciences · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
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  15. 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

6 authors at 4 institutions in 2 countries.

H-G MoonDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Z QinDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
T QuanDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
L XieDepartment of Respiratory Medicine, Chinese PLA General Hospital, Beijing, China.
C S Dela CruzDepartment of Pulmonary, Critical Care and Sleep Medicine, Yale University, New Haven, Connecticut, USA.
Y JinDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Brigham and Women's Hospital · USUniversity of Michigan · USChinese PLA General Hospital · CNYale University · US

Funding

Cross talk between cav-1 and flot1 in lung injuryR01HL102076 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI JIN, YANG · 2011 to 2015
$2.1M
Host-Pneumococcal Interaction in the LungR01HL126094 · NHLBI · YALE UNIVERSITY · PI DELA CRUZ, CHARLES S · 2015 to 2019
$2.1M
Mechanistic insights into the systemic inflammation and organ failure in sepsisR01GM111313 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI JIN, YANG · 2014 to 2017
$1.3M
NHLBI NIH HHS R01 HL102076NHLBI NIH HHS R01 HL126094NIGMS NIH HHS R01 GM111313
6 · The paper itself

Abstract

To defend against pulmonary infections, lung epithelial cells are equipped with complex innate immunity closely linked to inflammation. Dysregulated innate immunity/inflammation leads to self-perpetuating lung injury. The CpG motif in bacterial DNA is one of the factors involved in bacterial infection-associated inflammation. Bacterial DNA and synthetic CpG oligonucleotide (ODN) induced CCN1 secretion from lung epithelial cells, functioning as a potential "braking" signal to prevent uncontrolled inflammatory responses. CpG ODN-induced endoplasmic reticulum (ER) stress resulted in Src-Y527 phosphorylation (pY527) and Src/CCN1 vWF domain dissociation. Src-Y527 activated caveolin-1 (cav-1) phosphorylation at Y14 and then modulated CCN1 secretion via pCav-1 interaction with the CCN1 IGFbp domain. Functionally, secreted CCN1 promoted anti-inflammatory cytokine interleukin (IL)-10 release from epithelial cells via integrin αVβ6-PKC, and this subsequently suppressed tumor necrosis factor (TNF)-α, macrophage inflammatory protein 2 (MIP-2)-2 secretion and neutrophil infiltration in the lungs. Collectively, bacterial DNA/CpG ODN-stimulated CCN1 secretion via the BiP/GRP78-Src(Y527)-JNK-Cav-1(Y14) pathway and CpG-induced CCN1 conferred anti-inflammatory roles. Our studies suggested a novel paradigm by which the lung epithelium maintains innate immune homeostasis after bacterial infection.

Indexed as

HomeostasisImmunity, InnateAlveolar Epithelial CellsAnimalsAntigens, NeoplasmCaveolin 1Cysteine-Rich Protein 61CytokinesDisease Models, AnimalDNA, BacterialEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressInflammation MediatorsIntegrinsInterleukin-10MiceAntigens, NeoplasmCaveolin 1CPG-oligonucleotideCysteine-Rich Protein 61CytokinesDNA, BacterialEndoplasmic Reticulum Chaperone BiPHspa5 protein, mouseInflammation Mediatorsintegrin alphavbeta6IntegrinsInterleukin-10OligodeoxyribonucleotidesProto-Oncogene Proteins pp60(c-src)

Identifiers

PMID25005359
PMCPMC4289128
OpenAlexW2162207794

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.