Evidence map›Paper›PMID 31937554›Full record

ArticleThorax2020

RAGE-induced ILC2 expansion in acute lung injury due to haemorrhagic shock.

Kai Zhang, Yue Jin, Dengming Lai, Jieyan Wang, Yang Wang, Xiaoliang Wu, Melanie Scott, Yuehua Li, Jinchao Hou, Timothy Billiar and 4 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Thorax, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

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  12. Emerging Effects of IL-33 on COVID-19.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Kai Zhang *Department of Anesthesiology and Intensive Care, Zhejiang University School of Medicine First Affiliated Hospital, Hangzhou, Zhejiang, China.
Yue Jin *Department of Anesthesiology and Intensive Care, Zhejiang University School of Medicine First Affiliated Hospital, Hangzhou, Zhejiang, China.
Dengming LaiDepartment of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Jieyan WangDepartment of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Yang WangDepartment of Anesthesiology and Intensive Care, Zhejiang University School of Medicine First Affiliated Hospital, Hangzhou, Zhejiang, China.
Xiaoliang WuDepartment of Anesthesiology and Intensive Care, Zhejiang University School of Medicine First Affiliated Hospital, Hangzhou, Zhejiang, China.
Melanie ScottDepartment of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Yuehua LiDepartment of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Jinchao HouDepartment of Anesthesiology and Intensive Care, Zhejiang University School of Medicine First Affiliated Hospital, Hangzhou, Zhejiang, China.
Timothy BilliarDepartment of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Mark WilsonDepartment of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Qiang ShuDepartment of Thoracic and Cardiovascular Surgery, Zhejiang University School of Medicine Children's Hospital, Hangzhou, Zhejiang, China.
Xiangming FangDepartment of Anesthesiology and Intensive Care, Zhejiang University School of Medicine First Affiliated Hospital, Hangzhou, Zhejiang, China jif7@pitt.edu xmfang@zju.edu.cn.
Jie FanDepartment of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA jif7@pitt.edu xmfang@zju.edu.cn.
University of Pittsburgh · USFirst Affiliated Hospital Zhejiang University · CNChildren's Hospital of Zhejiang University · CN

Funding

IMPROVEMENT OF ORGAN FUNCTION AFTER SEVERE HYPOVOLEMIAR01HL076179 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2004 to 2026
$7.6M
Inflammasome activation in trauma-hemorrhagic shockR01GM102146 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SCOTT, MELANIE J. · 2013 to 2025
$4.3M
Cell Priming, Receptor Cross-Talk, and Acute Lung InjuryR01HL079669 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FAN, JIE, WILSON, MARK A. · 2005 to 2019
$4.0M
Macrophage Pyroptosis Mechanism of Post-Trauma Acute Lung InjuryR01HL139547 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FAN, JIE · 2018 to 2021
$1.6M
Cell Death Mechanism of Acute Lung Injury in SepsisI01BX002729 · VA · VETERANS HEALTH ADMINISTRATION · PI FAN, JIE · 2015 to 2020
–
BLR&D Research Career Scientist Award ApplicationIK6BX004211 · VA · VETERANS HEALTH ADMINISTRATION · PI FAN, JIE · 2018 to 2022
–
BLRD VA I01 BX002729BLRD VA IK6 BX004211NHLBI NIH HHS R01 HL076179NHLBI NIH HHS R01 HL079669NHLBI NIH HHS R01 HL139547NIGMS NIH HHS R01 GM102146
6 · The paper itself

Abstract

backgroundType 2 immune dysfunction contributes to acute lung injury and lethality following haemorrhagic shock (HS) and trauma. Group 2 innate lymphoid cells (ILC2s) play a significant role in the regulation of type 2 immune responses. However, the role of ILC2 in post-HS acute lung injury and the underlying mechanism has not yet been elucidated.

objectiveTo investigate the regulatory role of ILC2s in HS-induced acute lung injury and the underlying mechanism in patients and animal model.

methodsCirculating markers of type 2 immune responses in patients with HS and healthy controls were characterised. Using a murine model of HS, the role of high-mobility group box 1 (HMGB1)-receptor for advanced glycation end products (RAGE) signalling in regulation of ILC2 proliferation, survival and function was determined. And the role of ILC2 in inducing type 2 immune dysfunction was assessed as well.

resultsThe number of ILC2s was significantly increased in the circulation of patients with HS that was correlated with the increase in the markers of type 2 immune responses in the patients. Animal studies showed that HMGB1 acted via RAGE to induce ILC2 accumulation in the lungs by promoting ILC2 proliferation and decreasing ILC2 death. The expansion of ILC2s resulted in type 2 cytokines secretion and eosinophil infiltration in the lungs, both of which contributed to lung injury after HS.

conclusionsThese results indicate that HMGB1-RAGE signalling plays a critical role in regulating ILC2 biological function that aggravates type 2 lung inflammation following HS.

Indexed as

Acute Lung InjuryAnimalsAntigens, NeoplasmCase-Control StudiesCell ProliferationCell SurvivalDisease Models, AnimalEosinophilsFemaleHMGB1 ProteinHumansImmunity, InnateInterleukinsLymphocyte CountLymphocytesMaleAger protein, mouseAntigens, NeoplasmHMGB1 ProteinHMGB1 protein, humanHMGB1 protein, mouseInterleukinsMitogen-Activated Protein KinasesMOK protein, humanReceptor for Advanced Glycation End ProductsARDScritical carecytokine biologyinnate immunity

Identifiers

PMID31937554
PMCPMC7063398
OpenAlexW3000525524

What OpenQuestion holds

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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.