Evidence map›Paper›PMID 38747156›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Reducing Peptidoglycan Crosslinking by Chemical Modulator Reverts β-lactam Resistance in Methicillin-Resistant Staphylococcus aureus.

Ji-Hoon Kim, Yunmi Lee, Inseo Kim, JuOae Chang, Subin Hong, Na Kyung Lee, David Shum, Seongeun Baek, Wooseong Kim, Soojin Jang and 1 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
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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

11 authors.

Ji-Hoon KimSchool of Pharmacy, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Yunmi LeeAntibacterial Resistance Laboratory, Institut Pasteur Korea, Seongnam, 13488, Republic of Korea.
Inseo KimSchool of Pharmacy, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
JuOae ChangSchool of Pharmacy, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Subin HongSchool of Pharmacy, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Na Kyung LeeScreening Discovery Platform, Institut Pasteur Korea, Seongnam, 13488, Republic of Korea.
David ShumScreening Discovery Platform, Institut Pasteur Korea, Seongnam, 13488, Republic of Korea.
Seongeun BaekCollege of Pharmacy, Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul, 03760, Republic of Korea.
Wooseong KimCollege of Pharmacy, Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul, 03760, Republic of Korea.
Soojin JangAntibacterial Resistance Laboratory, Institut Pasteur Korea, Seongnam, 13488, Republic of Korea.
Wonsik LeeSchool of Pharmacy, Sungkyunkwan University, Suwon, 16419, Republic of Korea.ORCID 0000-0001-9707-4513

Funding

Korean government (MSIT) 2023M3A9G6057281Korean government (MSIT) NRF-2017M3A9G6068246Korean government (MSIT) NRF-2020M3A9H5104234Korean government (MSIT) NRF-RS-2023-00228746National Research Foundation of Korea
6 · The paper itself

Abstract

Small molecule can be utilized to restore the effectiveness of existing major classes of antibiotics against antibiotic-resistant bacteria. In this study, it is demonstrated that celastrol, a natural compound, can modify the bacterial cell wall and subsequently render bacteria more suceptible to β-lactam antibiotics. It is shown that celastrol leads to incomplete cell wall crosslinking by modulating levels of c-di-AMP, a secondary messenger, in methicillin-resistant Staphylococcus aureus (MRSA). This mechanism enables celastrol to act as a potentiator, effectively rendering MRSA susceptible to a range of penicillins and cephalosporins. Restoration of in vivo susceptibility of MRSA to methicillin is also demonstrated using a sepsis animal model by co-administering methicillin along with celastrol at a much lower amount than that of methicillin. The results suggest a novel approach for developing potentiators for major classes of antibiotics by exploring molecules that re-program metabolic pathways to reverse β-lactam-resistant strains to susceptible strains.

Indexed as

Anti-Bacterial Agentsbeta-Lactam ResistanceMethicillin-Resistant Staphylococcus aureusPeptidoglycanAnimalsbeta-LactamsCell WallDisease Models, AnimalMiceMicrobial Sensitivity TestsPentacyclic TriterpenesStaphylococcal InfectionsTriterpenesAnti-Bacterial Agentsbeta-LactamscelastrolPentacyclic TriterpenesPeptidoglycanTriterpenesc‐di‐AMPcelastrolpeptidoglycanStaphylococcus aureusβ‐lactam resistance

Identifiers

PMID38747156
PMCPMC11267302

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.