Evidence map›Paper›PMID 31632392›Full record

ArticleFrontiers in immunology2019

Endogenous Uteroglobin as Intrinsic Anti-inflammatory Signal Modulates Monocyte and Macrophage Subsets Distribution Upon Sepsis Induced Lung Injury.

Andrea Janicova, Nils Becker, Baolin Xu, Sebastian Wutzler, Jan Tilmann Vollrath, Frank Hildebrand, Sabrina Ehnert, Ingo Marzi, Philipp Störmann, Borna Relja

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. 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
2.6field-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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Very Late Antigen-4: A Novel Receptor for Club Cell Secretory Protein 16 to Control Inflammation.American journal of respiratory and critical care medicine · 2021
    Article
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  16. Club Cell Protein 16 Attenuates CD16Journal of immunology research · 2021
    Article
  17. Article
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  20. Coexistence of micro-inflammatory and macrophage phenotype abnormalities in chronic kidney disease.International journal of clinical and experimental pathology · 2020
    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.

Andrea JanicovaDepartment of Trauma, Hand and Reconstructive Surgery, Goethe University, Frankfurt, Germany.
Nils BeckerDepartment of Trauma, Hand and Reconstructive Surgery, Goethe University, Frankfurt, Germany.
Baolin XuDepartment of Trauma, Hand and Reconstructive Surgery, Goethe University, Frankfurt, Germany.
Sebastian WutzlerOrthopedic and Trauma Surgery, Helios Horst Schmidt Clinic, Wiesbaden, Germany.
Jan Tilmann VollrathDepartment of Trauma, Hand and Reconstructive Surgery, Goethe University, Frankfurt, Germany.
Frank HildebrandDepartment of Trauma Surgery, RWTH University, Aachen, Germany.
Sabrina EhnertDepartment of Trauma and Reconstructive Surgery, Siegfried Weller Research Institute, BG Trauma Center Tuebingen, Eberhard Karls University Tuebingen, Tuebingen, Germany.
Ingo MarziDepartment of Trauma, Hand and Reconstructive Surgery, Goethe University, Frankfurt, Germany.
Philipp StörmannDepartment of Trauma, Hand and Reconstructive Surgery, Goethe University, Frankfurt, Germany.
Borna ReljaDepartment of Trauma, Hand and Reconstructive Surgery, Goethe University, Frankfurt, Germany.
Goethe University Frankfurt · DEHelios Dr. Horst Schmidt Kliniken Wiesbaden · DERWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a serious clinical condition which can cause life-threatening organ dysfunction, and has limited therapeutic options. The paradigm of limiting excessive inflammation and promoting anti-inflammatory responses is a simplified concept. Yet, the absence of intrinsic anti-inflammatory signaling at the early stage of an infection can lead to an exaggerated activation of immune cells, including monocytes and macrophages. There is emerging evidence that endogenous molecules control those mechanisms. Here we aimed to identify and describe the dynamic changes in monocyte and macrophage subsets and lung damage in CL57BL/6N mice undergoing blunt chest trauma with subsequent cecal ligation and puncture. We showed that early an increase in systemic and activated Ly6C Short Summary: Blunt chest injury is the third largest cause of death following major trauma, and ongoing excessive pro-inflammatory immune response entails high risk for the development of secondary complications, such as sepsis, with limited therapeutic options. In murine double hit trauma consisting of thoracic trauma and subsequent cecal ligation and puncture, we investigated the cytokine profile, pulmonary epithelial integrity and phenotypic shift of patrolling Ly6C

Indexed as

Acute Lung InjuryAnimalsBiomarkersCell MovementCell SurvivalImmunophenotypingMacrophagesMaleMiceMonocytesSepsisUteroglobinBiomarkersUteroglobinacute lung injuryCC16chest injuryCLPmacrophagesmonocytessepsisuteroglobin

Identifiers

PMID31632392
PMCPMC6779999
OpenAlexW2978084647

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.