Evidence map›Paper›PMID 34867912›Full record

ArticleFrontiers in microbiology2021

Comparative Proteomics Demonstrates Altered Metabolism Pathways in Cotrimoxazole- Resistant and Amikacin-Resistant

Chunmei Shen, Ying Shen, Hui Zhang, Maosuo Xu, Leqi He, Jingbo Qie

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 53% 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

5 citing papers in PubMed, 7 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

6 authors at 1 institution in 1 country.

Chunmei ShenDepartment of Hospital Infection Management, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Ying ShenDepartment of Hospital Infection Management, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Hui ZhangDepartment of Clinical Laboratory Medicine, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Maosuo XuDepartment of Clinical Laboratory Medicine, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Leqi HeDepartment of Clinical Laboratory Medicine, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Jingbo QieDepartment of Hospital Infection Management, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibiotic resistance (AMR) has always been a hot topic all over the world and its mechanisms are varied and complicated. Previous evidence revealed the metabolic slowdown in resistant bacteria, suggesting the important role of metabolism in antibiotic resistance. However, the molecular mechanism of reduced metabolism remains poorly understood, which inspires us to explore the global proteome change during antibiotic resistance. Here, the sensitive, cotrimoxazole-resistant, amikacin-resistant, and amikacin/cotrimoxazole -both-resistant KPN clinical isolates were collected and subjected to proteome analysis through liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). A deep coverage of 2,266 proteins were successfully identified and quantified in total, representing the most comprehensive protein quantification data by now. Further bioinformatic analysis showed down-regulation of tricarboxylic acid cycle (TCA) pathway and up-regulation of alcohol metabolic or glutathione metabolism processes, which may contribute to ROS clearance and cell survival, in drug-resistant isolates. These results indicated that metabolic pathway alteration was directly correlated with antibiotic resistance, which could promote the development of antibacterial drugs from "target" to "network." Moreover, combined with minimum inhibitory concentration (MIC) of cotrimoxazole and amikacin on different KPN isolates, we identified nine proteins, including garK, uxaC, exuT, hpaB, fhuA, KPN_01492, fumA, hisC, and aroE, which might contribute mostly to the survival of KPN under drug pressure. In sum, our findings provided novel, non-antibiotic-based therapeutics against resistant KPN.

Indexed as

antibiotic resistancebioinformaticscomparative proteomicsKlebsiella pneumoniae (K. pneumoniae)metabolism

Identifiers

PMID34867912
PMCPMC8637018
OpenAlexW3216189267

What OpenQuestion holds

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Registered trials

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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.