Evidence map›Paper›PMID 38816687›Full record

ArticleBMC microbiology2024

Peptidoglycan endopeptidase MepM of uropathogenic Escherichia coli contributes to competitive fitness during urinary tract infections.

Wen-Chun Huang, Ida Bagus Nyoman Putra Dwija, Masayuki Hashimoto, Jiunn-Jong Wu, Ming-Cheng Wang, Cheng-Yen Kao, Wei-Hung Lin, Shuying Wang, Ching-Hao Teng

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Article in BMC microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

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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.

Wen-Chun HuangInstitute of Molecular Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Ida Bagus Nyoman Putra DwijaDepartment of Clinical Microbiology, Faculty of Medicine, Udayana University, Denpasar, Bali, Indonesia.
Masayuki HashimotoInstitute of Molecular Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Jiunn-Jong WuDepartment of Medical Laboratory Science and Biotechnology, Asia University, Taichung, Taiwan.
Ming-Cheng WangDivision of Nephrology, Department of Internal Medicine, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.
Cheng-Yen KaoInstitute of Microbiology and Immunology, College of Life Sciences, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Wei-Hung LinDepartment of Internal Medicine, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.
Shuying WangInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan. sswang23@mail.ncku.edu.tw.
Ching-Hao TengInstitute of Molecular Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan. chteng@mail.ncku.edu.tw.

Funding

Ministry of Science and Technology, Taiwan MOST 108-2320-B-006-034-MY3National Science and Technology Council, Taiwan NSTC 111-2320-B-006-048-MY3National Science and Technology Council, Taiwan NSTC 112-2320-B-006 -020 -MY3
6 · The paper itself

Abstract

backgroundUrinary tract infections (UTIs) are common bacterial infections, primarily caused by uropathogenic Escherichia coli (UPEC), leading to significant health issues and economic burden. Although antibiotics have been effective in treating UPEC infections, the rise of antibiotic-resistant strains hinders their efficacy. Hence, identifying novel bacterial targets for new antimicrobial approaches is crucial. Bacterial factors required for maintaining the full virulence of UPEC are the potential target. MepM, an endopeptidase in E. coli, is involved in the biogenesis of peptidoglycan, a major structure of bacterial envelope. Given that the bacterial envelope confronts the hostile host environment during infections, MepM's function could be crucial for UPEC's virulence. This study aims to explore the role of MepM in UPEC pathogenesis.

resultsMepM deficiency significantly impacted UPEC's survival in urine and within macrophages. Moreover, the deficiency hindered the bacillary-to-filamentous shape switch which is known for aiding UPEC in evading phagocytosis during infections. Additionally, UPEC motility was downregulated due to MepM deficiency. As a result, the mepM mutant displayed notably reduced fitness in causing UTIs in the mouse model compared to wild-type UPEC.

conclusionsThis study provides the first evidence of the vital role of peptidoglycan endopeptidase MepM in UPEC's full virulence for causing UTIs. MepM's contribution to UPEC pathogenesis may stem from its critical role in maintaining the ability to resist urine- and immune cell-mediated killing, facilitating the morphological switch, and sustaining motility. Thus, MepM is a promising candidate target for novel antimicrobial strategies.

Indexed as

EndopeptidasesEscherichia coli InfectionsUrinary Tract InfectionsUropathogenic Escherichia coliAnimalsDisease Models, AnimalEscherichia coli ProteinsFemaleHumansMacrophagesMicePeptidoglycanVirulenceEndopeptidasesEscherichia coli ProteinsPeptidoglycanpeptidoglycan endopeptidaseMepMMepSPathogenesisPeptidoglycan endopeptidaseSprUPECUrinary tract infectionUropathogenic E. ColiUTIYebA

Identifiers

PMID38816687
PMCPMC11137974

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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.