{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T17:57:22Z","timestamp":1761155842431},"reference-count":63,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2014,12,1]],"date-time":"2014-12-01T00:00:00Z","timestamp":1417392000000},"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":[[2014,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Neisseria meningitidis<\/jats:named-content>\n            is the causative agent of meningococcal disease. Onset of meningococcal disease can be extremely rapid and can kill within a matter of hours. However, although a much-feared pathogen,\n            <jats:named-content content-type=\"genus-species\">Neisseria meningitidis<\/jats:named-content>\n            is frequently found in the nasopharyngeal mucosae of healthy carriers. The bacterial factors that distinguish disease- from carriage-associated meningococci are incompletely understood. Evidence suggesting that disruptions to the nasopharynx may increase the risk of acquiring meningococcal disease led us to evaluate the ability of disease- and carriage-associated meningococcal isolates to inhibit cell migration, using an\n            <jats:italic>in vitro<\/jats:italic>\n            assay for wound repair. We found that disease-associated isolates in our collection inhibited wound closure, while carriage-associated isolates were more variable, with many isolates not inhibiting wound repair at all. For isolates selected for further study, we found that actin morphology, such as presence of lamellipodia, correlated with cell migration. We demonstrated that multiple meningococcal virulence factors, including the type IV pili, are dispensable for inhibition of wound repair. Inhibition of wound repair was also shown to be an active process, i.e., requiring live bacteria undergoing active protein synthesis.\n          <\/jats:p>","DOI":"10.1128\/iai.02001-14","type":"journal-article","created":{"date-parts":[[2014,9,16]],"date-time":"2014-09-16T05:57:57Z","timestamp":1410847077000},"page":"5023-5034","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":5,"title":["Disease-Associated Neisseria meningitidis Isolates Inhibit Wound Repair in Respiratory Epithelial Cells in a Type IV Pilus-Independent Manner"],"prefix":"10.1128","volume":"82","author":[{"given":"Xiaoyun","family":"Ren","sequence":"first","affiliation":[{"name":"Institute of Environmental Science and Research, Kenepuru Science Centre, Porirua, New Zealand"},{"name":"School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joanna K.","family":"MacKichan","sequence":"additional","affiliation":[{"name":"Institute of Environmental Science and Research, Kenepuru Science Centre, Porirua, New Zealand"},{"name":"School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand"},{"name":"Centre for Biodiscovery, Victoria University of Wellington, Wellington, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.vaccine.2009.04.070"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1097\/01.inf.0000147642.85129.05"},{"key":"e_1_3_3_4_2","volume-title":"Topley and Wilson's microbiology and microbial infections","author":"Mietzner TA","year":"2010","unstructured":"MietznerTAMorseSA. 2010. 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