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Peer-reviewedCC BYBMC microbiology

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

4 affiliations
  1. 1Institute of Microbiology and Epizootics, School of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany. [email protected].
  2. 2Veterinary Centre for Resistance Research (TZR), School of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany.
  3. 3Institute of Microbiology, University of Veterinary Medicine Hannover, Bischofsholer Damm 15, 30173, Hannover, Germany.
  4. 4Institute of Microbiology and Epizootics, School of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany.

Abstract

Background

LepA 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.Methods

We 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.Results

The 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.Conclusion

These 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.

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BibTeX
@article{braetz2026contribution,
  title = {{The contribution of LepA to virulence and host cell invasion in Salmonella Typhimurium.}},
  author = {Sebastian Braetz and Andreas Nerlich and Marcus Fulde},
  journal = {BMC microbiology},
  year = {2026},
  month = oct,
  doi = {10.1186/s12866-026-05826-7},
  url = {https://europepmc.org/article/MED/42907766},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - The contribution of LepA to virulence and host cell invasion in Salmonella Typhimurium.
AU  - Sebastian Braetz
AU  - Andreas Nerlich
AU  - Marcus Fulde
PY  - 2026
DA  - 2026/10/22
JO  - BMC microbiology
DO  - 10.1186/s12866-026-05826-7
UR  - https://europepmc.org/article/MED/42907766
AB  - Background  LepA 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.Methods  We 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.Results  The 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.Conclusion  These 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.
SN  - 1471-2180
ER  -