Evidence map›Paper›PMID 33536477›Full record

ArticleScientific reports2021

IOX1 activity as sepsis therapy and an antibiotic against multidrug-resistant bacteria.

Su Jin Lee, Jueng Soo You, Amal Gharbi, Yong Joo Kim, Mi Suk Lee, Dong Hwan Kim, Keun Woo Lee, In Duk Jung, Yeong Min Park

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Su Jin Lee *Department of Immunology, Laboratory of Dendritic Cell Differentiation and Regulation, School of Medicine, Konkuk University, Chungju, Seoul, 380-701, Republic of Korea.
Jueng Soo You *Department of Biochemistry, School of Medicine, Konkuk University, Chungju, Seoul, 380-701, Republic of Korea.
Amal Gharbi *Dandi Bioscience Inc, 6Th Floor of Real Company, 66, Acha San-ro, Seongdong-gu, Seoul, Republic of Korea.
Yong Joo KimDandi Bioscience Inc, 6Th Floor of Real Company, 66, Acha San-ro, Seongdong-gu, Seoul, Republic of Korea.
Mi Suk LeeDandi Bioscience Inc, 6Th Floor of Real Company, 66, Acha San-ro, Seongdong-gu, Seoul, Republic of Korea.
Dong Hwan KimDivision of Life Science, Research Institute of Natural Science (RINS), Gyeongsang National University (GNU), 501 Jinju-daero, Jinju, 52828, Republic of Korea.
Keun Woo LeeDivision of Life Science, Research Institute of Natural Science (RINS), Gyeongsang National University (GNU), 501 Jinju-daero, Jinju, 52828, Republic of Korea.
In Duk JungDandi Bioscience Inc, 6Th Floor of Real Company, 66, Acha San-ro, Seongdong-gu, Seoul, Republic of Korea. jungid@dandibio.com.
Yeong Min ParkDepartment of Immunology, Laboratory of Dendritic Cell Differentiation and Regulation, School of Medicine, Konkuk University, Chungju, Seoul, 380-701, Republic of Korea. immun3023@kku.ac.kr.
Gyeongsang National University · KRKonkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is caused by organ dysfunction initiated by an unrestrained host immune response to infection. The emergence of antibiotic-resistant bacteria has rapidly increased in the last decades and has stimulated a firm research platform to combat infections caused by antibiotic-resistant bacteria that cannot be eradicated with conventional antibiotics. Strategies like epigenetic regulators such as lysine demethylase (Kdm) has received attention as a new target. Thus, we sought to investigate the epigenetic mechanisms in sepsis pathophysiology with the aim of discovering new concepts for treatment. A transcriptome analysis of dendritic cells during their inflammatory state identified Kdm as a critical molecule in sepsis regulation. Next, 8-hydroxyquinoline-5-carboxylic acid (IOX1) ability to control endotoxemia induced by Lipopolysaccharide and bacterial sepsis was demonstrated. IOX1 has been shown to regulate endotoxemia and sepsis caused by Escherichia coli and carbapenem-resistant Acinetobacter baumannii and has also contributed to the suppression of multidrug-resistant bacterial growth through the inhibition of DNA Gyrase. These findings show that IOX1 could be a component agent against bacterial sepsis by functioning as a broad-spectrum antibiotic with dual effects.

Indexed as

Acinetobacter baumanniiAcinetobacter InfectionsAnimalsAnti-Bacterial AgentsDendritic CellsDisease Models, AnimalDNA GyraseDrug Resistance, Multiple, BacterialEscherichia coliEscherichia coli InfectionsFemaleHistone DemethylasesHumansHydroxyquinolinesMiceMicrobial Sensitivity Tests5-carboxy-8-hydroxyquinolineAnti-Bacterial AgentsDNA GyraseHistone DemethylasesHydroxyquinolines

Identifiers

PMID33536477
PMCPMC7858575
OpenAlexW3126276265

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.