Evidence map›Paper›PMID 33333514›Full record

ArticleJournal of innate immunity2021

Double-Stranded RNA Dependent Kinase R Regulates Antibacterial Immunity in Sepsis.

Yanliang Yang, Lingli Xie, Yanjun Zhong, Xiaoli Zhong, Ran Meng, Qianqian Xue, Fang Liang, Kai Zhao, Yiting Tang

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

Article in Journal of innate immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
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 1 institution in 1 country.

Yanliang YangDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha, China.
Lingli XieDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, Central South University, Changsha, China.
Yanjun ZhongThe Second Xiangya Hospital, Central South University, Changsha, China.
Xiaoli ZhongDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, Central South University, Changsha, China.
Ran MengDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, Central South University, Changsha, China.
Qianqian XueDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, Central South University, Changsha, China.
Fang LiangDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, Central South University, Changsha, China.
Kai ZhaoDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, Central South University, Changsha, China.
Yiting TangDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha, China, yitingtang@csu.edu.cn.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Double-stranded RNA dependent kinase R (PKR) is originally identified as an intracellular sensor of viral infection, but its role in bacterial infection remains largely unknown. Here we report that PKR was an important regulator of antibacterial immunity in sepsis. Genetic deletion of PKR or pharmacological inhibition of its kinase activity markedly increased bacterial loads, organ injury, and mortality in polymicrobial infection induced by cecal ligation and puncture (CLP). In contrast, PKR deficiency or inhibition did not affect bacterial loads, organ injury, or mortality when mice were systemically challenged with Escherichia coli, an abundant microbe in the gastrointestinal tract. PKR deficiency or inhibition markedly decreased the release of interleukin (IL)-1β after CLP. Defect in IL-1 signaling phenocopied PKR deficiency or inhibition in CLP-induced bacterial sepsis. Taken together, these findings identified a critical role of the PKR signaling pathway in antibacterial immunity.

Indexed as

AnimalsCecumCells, CulturedDisease Models, AnimaleIF-2 KinaseEscherichia coliEscherichia coli InfectionsHumansImmunity, InnateIndolesInterleukin-1betaMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutRNA, Double-StrandedeIF-2 KinaseGW 506033XIndolesInterleukin-1betaRNA, Double-StrandedThiazolesBacterial sepsisDouble-stranded RNA dependent kinase RInterleukin-1

Identifiers

PMID33333514
PMCPMC7879320
OpenAlexW3112059864

What OpenQuestion holds

Textmetadata
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.