Evidence map›Paper›PMID 42907766›Full record

ArticleBMC microbiology2026

The contribution of LepA to virulence and host cell invasion in Salmonella Typhimurium.

Sebastian Braetz, Andreas Nerlich, Marcus Fulde

Abstract read
In one paragraph

Article in BMC microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Sebastian BraetzInstitute of Microbiology and Epizootics, School of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany. sebastian.braetz@fu-berlin.de.
Andreas NerlichVeterinary Centre for Resistance Research (TZR), School of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany.
Marcus FuldeInstitute of Microbiology and Epizootics, School of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLepA is one of the most conserved proteins and is found in nearly all bacteria as well as in eukaryotes. Mutation of lepA increases antibiotic tolerance in Escherichia coli, Salmonella, and rifampicin-resistant clinical mycobacterial isolates. However, the physiological function and its role in virulence of LepA remain elusive, particularly considering that LepA is non-essential under laboratory conditions.

methodsWe investigated the lepA gene of Salmonella Typhimurium for its role in bacterial invasion of host cells. Invasion assays using lepA mutants were performed in macrophages (J774) and epithelial cells (Caco-2 and HT29-MTX), both in the presence and absence of mucus. In addition, virulence gene induction, motility, and pathogenicity in a Galleria mellonella infection model were assessed.

resultsThe lepA deletion strain showed reduced invasion in all cell types regardless of mucus, indicating its essential role in the invasion process and in the initial survival within macrophages. Deletion of lepA also resulted in decreased induction of virulence-associated genes and reduced pathogenicity in Galleria mellonella.

conclusionThese findings provide important insights into the molecular determinants of Salmonella Typhimurium virulence and contribute to a deeper understanding of the conservation of LepA across organisms.

Indexed as

Bacterial ProteinsSalmonella typhimuriumVirulence FactorsAnimalsCaco-2 CellsCell LineEpithelial CellsHost TropismHumansMacrophagesMothsSalmonella InfectionsVirulenceBacterial ProteinsVirulence Factorsbacterial invasionGalleria mellonella infection modelhost-pathogen interactionLepASalmonellavirulence regulation

Identifiers

PMID42907766
PMCPMC13689319

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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.