Evidence map›Paper›PMID 34950139›Full record

ArticleFrontiers in immunology2021

Citrullinated Histone H3 Mediates Sepsis-Induced Lung Injury Through Activating Caspase-1 Dependent Inflammasome Pathway.

Yuzi Tian, Patrick Li, Zhenyu Wu, Qiufang Deng, Baihong Pan, Kathleen A Stringer, Hasan B Alam, Theodore J Standiford, Yongqing Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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  20. [Mechanism of Extracellular Histone-Induced Endothelial Dysfunction Leading to Sepsis-Induced Acute Respiratory Distress Syndrome].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    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

9 authors at 3 institutions in 2 countries.

Yuzi TianDepartment of Rheumatology and Immunology, Xiangya Hospital, Central South University, Changsha, China.
Patrick LiDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, United States.
Zhenyu WuDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, United States.
Qiufang DengDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, United States.
Baihong PanDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, United States.
Kathleen A StringerDepartment of Clinical Pharmacy, College of Pharmacy, University of Michigan, Ann Arbor, MI, United States.
Hasan B AlamDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, United States.
Theodore J StandifordDivision of Pulmonary and Critical Care Medicine, University of Michigan Medical Center, Ann Arbor, MI, United States.
Yongqing LiDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, United States.
University of Michigan–Ann Arbor · USMichigan Medicine · USSecond Xiangya Hospital of Central South University · CN

Funding

PAD2 and CitH3 in Pathogenesis of Sepsis-induced ALIR01HL155116 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALAM, HASAN B, LI, YONGQING · 2021 to 2024
$2.1M
NHLBI NIH HHS R01 HL155116
6 · The paper itself

Abstract

Sepsis is a life-threatening organ dysfunction caused by dysregulated host response to infection that often results in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). An emerging mechanism of sepsis-induced ARDS involves neutrophils/macrophages undergoing cell death, releasing nuclear histones to cause tissue damage that exacerbates pulmonary injury. While published studies focus on unmodified histones, little is known about the role of citrullinated histone H3 (CitH3) in the pathogenesis of sepsis and ALI. In this study, we found that levels of CitH3 were elevated in the patients with sepsis-induced ARDS and correlated to PaO2/FiO2 in septic patients. Systematic administration of CitH3 peptide in mice provoked Caspase-1 activation in the lung tissue and caused ALI. Neutralization of CitH3 with monoclonal antibody improved survival and attenuated ALI in a mouse sepsis model. Furthermore, we demonstrated that CitH3 induces ALI through activating Caspase-1 dependent inflammasome in bone marrow derived macrophages and bone marrow derived dendritic cells. Our study suggests that CitH3 is an important mediator of inflammation and mortality during sepsis-induced ALI.

Indexed as

Acute Lung InjuryAnimalsBronchoalveolar Lavage FluidCaspase 1Cells, CulturedCitrullinationDendritic CellsHistonesHumansInflammasomesMacrophagesMaleMiceMice, Inbred C57BLPeptidesRandomized Controlled Trials as TopicCaspase 1HistonesInflammasomesPeptidesacute lung injuryCaspase-1 (CASP1)citrullinated histone H3 (CitH3)inflammasomesepsis

Identifiers

PMID34950139
PMCPMC8688857
OpenAlexW4200138005

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.