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Mutation of\n                      <jats:italic>lepA<\/jats:italic>\n                      increases antibiotic tolerance in\n                      <jats:italic>Escherichia coli<\/jats:italic>\n                      ,\n                      <jats:italic>Salmonella<\/jats:italic>\n                      , 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.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We investigated the\n                      <jats:italic>lepA<\/jats:italic>\n                      gene of\n                      <jats:italic>Salmonella<\/jats:italic>\n                      Typhimurium for its role in bacterial invasion of host cells. Invasion assays using\n                      <jats:italic>lepA<\/jats:italic>\n                      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\n                      <jats:italic>Galleria mellonella<\/jats:italic>\n                      infection model were assessed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The\n                      <jats:italic>lepA<\/jats:italic>\n                      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\n                      <jats:italic>lepA<\/jats:italic>\n                      also resulted in decreased induction of virulence-associated genes and reduced pathogenicity in\n                      <jats:italic>Galleria mellonella<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      These findings provide important insights into the molecular determinants of\n                      <jats:italic>Salmonella<\/jats:italic>\n                      Typhimurium virulence and contribute to a deeper understanding of the conservation of LepA across organisms.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12866-026-05826-7","type":"journal-article","created":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T02:05:08Z","timestamp":1792634708000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The contribution of LepA to virulence and host cell invasion in Salmonella Typhimurium"],"prefix":"10.1186","volume":"26","author":[{"given":"Sebastian","family":"Braetz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Nerlich","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcus","family":"Fulde","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,10,22]]},"reference":[{"key":"5826_CR1","doi-asserted-by":"publisher","first-page":"284","DOI":"10.1080\/21553769.2015.1051243","volume":"8","author":"SK Eng","year":"2015","unstructured":"Eng SK, Pusparajah P, Ab Mutalib NS, Ser HL, Chan KG, Lee LH. 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