Evidence map›Paper›PMID 28611371›Full record

ArticleScientific reports2017

Ohmyungsamycins promote antimicrobial responses through autophagy activation via AMP-activated protein kinase pathway.

Tae Sung Kim, Yern-Hyerk Shin, Hye-Mi Lee, Jin Kyung Kim, Jin Ho Choe, Ji-Chan Jang, Soohyun Um, Hyo Sun Jin, Masaaki Komatsu, Guang-Ho Cha and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 42 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

13 authors at 5 institutions in 2 countries.

Tae Sung KimDepartment of Microbiology, Chungnam National University School of Medicine, Daejeon, 35015, South Korea.
Yern-Hyerk ShinNatural Products Research Institute, College of Pharmacy, Seoul National University, Seoul, 08826, South Korea.
Hye-Mi LeeDepartment of Microbiology, Chungnam National University School of Medicine, Daejeon, 35015, South Korea.
Jin Kyung KimDepartment of Microbiology, Chungnam National University School of Medicine, Daejeon, 35015, South Korea.
Jin Ho ChoeDepartment of Microbiology, Chungnam National University School of Medicine, Daejeon, 35015, South Korea.
Ji-Chan JangMolecular Mechanism of Antibiotics, Division of Life Science, Research Institute of Life Science, Gyeongsang National University, Jinju, 52828, South Korea.
Soohyun UmNatural Products Research Institute, College of Pharmacy, Seoul National University, Seoul, 08826, South Korea.
Hyo Sun JinDepartment of Microbiology, Chungnam National University School of Medicine, Daejeon, 35015, South Korea.
Masaaki KomatsuDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Niigata, 9518510, Japan.
Guang-Ho ChaDepartment of Infection Biology, Chungnam National University School of Medicine, Daejeon, 35015, South Korea.
Han-Jung ChaeDepartment of Pharmacology, Chonbuk National University Medical School, Jeonju, 54907, South Korea.
Dong-Chan OhNatural Products Research Institute, College of Pharmacy, Seoul National University, Seoul, 08826, South Korea. dongchanoh@snu.ac.kr.
Eun-Kyeong JoDepartment of Microbiology, Chungnam National University School of Medicine, Daejeon, 35015, South Korea. hayoungj@cnu.ac.kr.
Chungnam National University · KRSeoul National University · KRGyeongsang National University · KRJeonbuk National University · KRNiigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The induction of host cell autophagy by various autophagy inducers contributes to the antimicrobial host defense against Mycobacterium tuberculosis (Mtb), a major pathogenic strain that causes human tuberculosis. In this study, we present a role for the newly identified cyclic peptides ohmyungsamycins (OMS) A and B in the antimicrobial responses against Mtb infections by activating autophagy in murine bone marrow-derived macrophages (BMDMs). OMS robustly activated autophagy, which was essentially required for the colocalization of LC3 autophagosomes with bacterial phagosomes and antimicrobial responses against Mtb in BMDMs. Using a Drosophila melanogaster-Mycobacterium marinum infection model, we showed that OMS-A-induced autophagy contributed to the increased survival of infected flies and the limitation of bacterial load. We further showed that OMS triggered AMP-activated protein kinase (AMPK) activation, which was required for OMS-mediated phagosome maturation and antimicrobial responses against Mtb. Moreover, treating BMDMs with OMS led to dose-dependent inhibition of macrophage inflammatory responses, which was also dependent on AMPK activation. Collectively, these data show that OMS is a promising candidate for new anti-mycobacterial therapeutics by activating antibacterial autophagy via AMPK-dependent signaling and suppressing excessive inflammation during Mtb infections.

Indexed as

AutophagyAMP-Activated Protein Kinase KinasesAnimalsAnti-Bacterial AgentsCells, CulturedDepsipeptidesHumansMacrophagesMiceMice, Inbred C57BLMycobacterium InfectionsMycobacterium tuberculosisPeptides, CyclicProtein KinasesStreptomycesAMP-Activated Protein Kinase KinasesAnti-Bacterial AgentsDepsipeptidesohmyungsamycin Aohmyungsamycin BPeptides, CyclicProtein Kinases

Identifiers

PMID28611371
PMCPMC5469788
OpenAlexW2623037906

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.