{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:29:19Z","timestamp":1792024159746,"version":"4.4.0"},"reference-count":34,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2012,7,1]],"date-time":"2012-07-01T00:00:00Z","timestamp":1341100800000},"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":[[2012,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Neisseria meningitidis<\/jats:named-content>\n            is a major cause of sepsis and bacterial meningitis worldwide. This bacterium expresses type IV pili (Tfp), which mediate important virulence traits such as the formation of bacterial aggregates, host cell adhesion, twitching motility, and DNA uptake. The meningococcal PilT protein is a hexameric ATPase that mediates pilus retraction. The PilU protein is produced from the\n            <jats:italic>pilT-pilU<\/jats:italic>\n            operon and shares a high degree of homology with PilT. The function of PilT in Tfp biology has been studied extensively, whereas the role of PilU remains poorly understood. Here we show that\n            <jats:italic>pilU<\/jats:italic>\n            mutants have delayed microcolony formation on host epithelial cells compared to the wild type, indicating that bacterium-bacterium interactions are affected. In normal human serum, the\n            <jats:italic>pilU<\/jats:italic>\n            mutant survived at a higher rate than that for wild-type bacteria. However, in a murine model of disease, mice infected with the\n            <jats:italic>pilT<\/jats:italic>\n            mutant demonstrated significantly reduced bacterial blood counts and survived at a higher rate than that for mice infected with the wild type. Infection of mice with the\n            <jats:italic>pilU<\/jats:italic>\n            mutant resulted in a trend of lower bacteremia, and still a significant increase in survival, than that of the wild type. In conclusion, these data suggest that PilU promotes timely microcolony formation and that both PilU and PilT are required for full bacterial virulence.\n          <\/jats:p>","DOI":"10.1128\/iai.06354-11","type":"journal-article","created":{"date-parts":[[2012,4,17]],"date-time":"2012-04-17T05:26:55Z","timestamp":1334640415000},"page":"2538-2547","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":30,"title":["Loss of Meningococcal PilU Delays Microcolony Formation and Attenuates Virulence\n            <i>In Vivo<\/i>"],"prefix":"10.1128","volume":"80","author":[{"given":"Jens","family":"Eriksson","sequence":"first","affiliation":[{"name":"Department of Genetics, Microbiology and Toxicology, Stockholm University, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olaspers Sara","family":"Eriksson","sequence":"additional","affiliation":[{"name":"Department of Genetics, Microbiology and 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