Evidence map›Paper›PMID 33117383›Full record

ArticleFrontiers in immunology2020

CCR2 Mediates Chronic LPS-Induced Pulmonary Inflammation and Hypoalveolarization in a Murine Model of Bronchopulmonary Dysplasia.

Tracy X Cui, Alexander E Brady, Christina T Fulton, Ying-Jian Zhang, Liza M Rosenbloom, Adam M Goldsmith, Bethany B Moore, Antonia P Popova

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-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

27 citing papers in PubMed, 44 citations in OpenAlex.

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  17. Two-year outcomes following a randomised platelet transfusion trial in preterm infants.Archives of disease in childhood. Fetal and neonatal edition · 2023
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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.

Tracy X CuiDivision of Pediatric Pulmonology, Department of Pediatrics, University of Michigan Medical School, Ann Arbor, MI, United States.
Alexander E BradyDivision of Pediatric Pulmonology, Department of Pediatrics, University of Michigan Medical School, Ann Arbor, MI, United States.
Christina T FultonDivision of Pediatric Pulmonology, Department of Pediatrics, University of Michigan Medical School, Ann Arbor, MI, United States.
Ying-Jian ZhangDivision of Pediatric Pulmonology, Department of Pediatrics, University of Michigan Medical School, Ann Arbor, MI, United States.
Liza M RosenbloomDivision of Pediatric Pulmonology, Department of Pediatrics, University of Michigan Medical School, Ann Arbor, MI, United States.
Adam M GoldsmithDivision of Pediatric Pulmonology, Department of Pediatrics, University of Michigan Medical School, Ann Arbor, MI, United States.
Bethany B MooreDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, United States.
Antonia P PopovaDivision of Pediatric Pulmonology, Department of Pediatrics, University of Michigan Medical School, Ann Arbor, MI, United States.
University of Michigan–Ann Arbor · US

Funding

Early life hyperoxic exposure, lung innate immune responses, bronchopulmonary dysplasia and asthmaR01HL140572 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI POPOVA, ANTONIA PETROVA · 2018 to 2022
$1.9M
NHLBI NIH HHS R01 HL140572
6 · The paper itself

Abstract

The histopathology of bronchopulmonary dysplasia (BPD) includes hypoalveolarization and interstitial thickening due to abnormal myofibroblast accumulation. Chorioamnionitis and sepsis are major risk factors for BPD development. The cellular mechanisms leading to these lung structural abnormalities are poorly understood. We used an animal model with repeated lipopolysaccharide (LPS) administration into the airways of immature mice to simulate prolonged airway exposure to gram-negative bacteria, focusing on the role of C-C chemokine receptor type 2-positive (CCR2+) exudative macrophages (ExMf). Repetitive LPS exposure of immature mice induced persistent hypoalveolarization observed at 4 and 18 days after the last LPS administration. LPS upregulated the expression of lung pro-inflammatory cytokines (TNF-

Indexed as

AnimalsBronchopulmonary DysplasiaCells, CulturedChronic DiseaseCytokinesDisease Models, AnimalHumansInflammationInflammation MediatorsLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLMice, KnockoutPulmonary AlveoliReceptor, Platelet-Derived Growth Factor alphaCcr2 protein, mouseCytokinesInflammation MediatorsLipopolysaccharidesReceptor, Platelet-Derived Growth Factor alphaReceptors, CCR2bronchopulmonary dysplasiaCCR2inflammationmacrophagesprematurity

Identifiers

PMID33117383
PMCPMC7573800
OpenAlexW3092172321

What OpenQuestion holds

Textmetadata
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.