{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T19:52:47Z","timestamp":1790970767423,"version":"4.1.0"},"reference-count":28,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2007,1,1]],"date-time":"2007-01-01T00:00:00Z","timestamp":1167609600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Listeria monocytogenes<\/jats:italic>is a bacterial pathogen that multiplies in the cytosol of host cells and spreads directly from cell to cell by using an actin-based mechanism of motility. The broad-range phospholipase C (PC-PLC) of<jats:italic>L. monocytogenes<\/jats:italic>contributes to bacterial escape from vacuoles formed upon cell-to-cell spread. PC-PLC is made as an inactive proenzyme whose activation requires cleavage of an N-terminal propeptide. During infection, PC-PLC is activated specifically in acidified vacuoles. To assess the importance of compartmentalizing PC-PLC activity during infection, we created a mutant that makes constitutively active PC-PLC (the<jats:italic>plcB<\/jats:italic>\u0394pro mutant). Results from intracellular growth and cell-to-cell spread assays showed that the<jats:italic>plcB<\/jats:italic>\u0394pro mutant was sensitive to gentamicin, suggesting that unregulated PC-PLC activity causes damage to host cell membranes. This was confirmed by the observation of a twofold increase in staining of live infected cells by a non-membrane-permeant DNA fluorescent dye. However, membrane damage was not sufficient to cause cell lysis and was dependent on bacterial cell-to-cell spread, suggesting that damage was localized to bacterium-containing filopodia. Using an in vivo competitive infection assay, we observed that the<jats:italic>plcB<\/jats:italic>\u0394pro mutant was outcompeted up to 200-fold by the wild-type strain in BALB\/c mice. Virulence attenuation was greater when mice were infected orally than when they were infected intravenously, presumably because the<jats:italic>plcB<\/jats:italic>\u0394pro mutant was initially outcompeted in the intestines, reducing the number of mutant bacteria reaching the liver and spleen. Together, these results emphasize the importance for<jats:italic>L. monocytogenes<\/jats:italic>virulence of compartmentalizing the activity of PC-PLC during infection.<\/jats:p>","DOI":"10.1128\/iai.01001-06","type":"journal-article","created":{"date-parts":[[2006,12,20]],"date-time":"2006-12-20T23:51:25Z","timestamp":1166658685000},"page":"44-51","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":37,"title":["Compartmentalization of the Broad-Range Phospholipase C Activity to the Spreading Vacuole Is Critical for<i>Listeria monocytogenes<\/i>Virulence"],"prefix":"10.1128","volume":"75","author":[{"given":"P. S. 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