{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T14:17:47Z","timestamp":1785421067327,"version":"3.56.0"},"reference-count":44,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T00:00:00Z","timestamp":1775520000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T00:00:00Z","timestamp":1775520000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100004063","name":"Knut och Alice Wallenbergs Stiftelse","doi-asserted-by":"publisher","award":["WCMTM"],"award-info":[{"award-number":["WCMTM"]}],"id":[{"id":"10.13039\/501100004063","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004359","name":"Swedish Research Council","doi-asserted-by":"publisher","award":["2020-04299"],"award-info":[{"award-number":["2020-04299"]}],"id":[{"id":"10.13039\/501100004359","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002794","name":"Cancerfonden","doi-asserted-by":"publisher","award":["22-2409"],"award-info":[{"award-number":["22-2409"]}],"id":[{"id":"10.13039\/501100002794","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2026,4,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Antibiotic resistance is a critical public health issue, causing resistant bacterial strains to be increasingly difficult to control. Antivirulence therapies, which target bacterial virulence factors rather than kill bacteria, present a promising approach. Sortase enzymes, particularly SrtA, are crucial for gram-positive bacterial virulence by anchoring surface proteins essential for bacterial adhesion and biofilm formation to the bacterial outer cell wall. This study evaluates the selectivity of the peptidomimetic inhibitor BzLPRDSar toward various gram-positive bacteria. The BzLPRDSar significantly inhibited biofilm formation in multidrug-resistant\n                      <jats:italic toggle=\"yes\">Staphylococcus aureus<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Staphylococcus epidermidis<\/jats:italic>\n                      . Conversely, it showed variable and generally lower selectivity to gram-positive species such as\n                      <jats:italic toggle=\"yes\">Enterococcus faecalis<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">Bacillus cereus<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">Streptococcus agalactiae<\/jats:italic>\n                      . The selectivity toward\n                      <jats:italic toggle=\"yes\">Staphylococcus<\/jats:italic>\n                      species is attributed to conserved structural elements in the SrtA enzyme, particularly the \u03b27\/\u03b28 loop region with a key tryptophan, likely facilitating strong binding interactions with the inhibitor.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      Antibiotic resistance is making it harder to treat bacterial infections, even with our strongest medicines. This study explores a new approach that does not aim to kill bacteria but instead disarms them by blocking the tools they use to cause disease. We focused on a bacterial enzyme called sortase A (SrtA), which helps harmful bacteria stick to surfaces and form protective layers called biofilms\u2014structures that make infections very difficult to treat. We tested a specially designed molecule, BzLPRDSar, and found it could stop biofilm formation in drug-resistant strains of\n                      <jats:italic toggle=\"yes\">Staphylococcus aureus<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Staphylococcus epidermidis<\/jats:italic>\n                      . It was less effective against other bacteria, likely because of differences in the SrtA enzyme sequences. Our findings suggest that targeting virulence rather than killing bacteria may offer a safer and more sustainable way to treat infections, especially those caused by bacteria that no longer respond to antibiotics.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/spectrum.02327-25","type":"journal-article","created":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T14:00:20Z","timestamp":1772546420000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["Targeted sortase A inhibition by novel peptidomimetic antivirulents against staphylococcal infections"],"prefix":"10.1128","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4621-0711","authenticated-orcid":false,"given":"Jordi C. 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