{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,18]],"date-time":"2023-10-18T19:32:05Z","timestamp":1697657525356},"reference-count":16,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2006,2,1]],"date-time":"2006-02-01T00:00:00Z","timestamp":1138752000000},"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":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2006,2]]},"abstract":"ABSTRACT<\/jats:title>\n \n Chlamydia<\/jats:italic>\n species are widely disseminated obligate intracellular pathogens that primarily cause urogenital, ocular, and respiratory infections. In these studies, we show that exposing mammalian cells to antibacterial agents prior to\n Chlamydia<\/jats:italic>\n inoculation protects the host cells against subsequent challenge by chlamydiae (the protective effect [PE]). Rifalazil exhibited a considerably stronger PE than did azithromycin, rifampin, doxycycline, and ofloxacin. Specifically, 0.002 \u03bcg\/ml rifalazil incubated for 1 day with a monolayer of McCoy cells was sufficient to protect against a challenge 2 days later with\n Chlamydia trachomatis<\/jats:italic>\n serovar D (UW-3). The PE was observed with five different mammalian cell lines and with a variety of\n C. trachomatis<\/jats:italic>\n and\n Chlamydia pneumoniae<\/jats:italic>\n isolates. The duration of the PE was 6 to 12 days for rifalazil (depending on the cell line), a maximum of 3 days for azithromycin, and less than a day for the other drugs tested. For rifalazil, the PE was shown to be mediated by inhibition of the chlamydial RNA polymerase since mutants with altered RNA polymerases had correspondingly altered PEs. These results suggest that rifalazil may be unique in its ability to prevent infection with obligate intracellular pathogens for a considerable time after treatment. This characteristic may be of particular public health value in reducing reinfection with chlamydiae.\n <\/jats:p>","DOI":"10.1128\/aac.50.2.439-444.2006","type":"journal-article","created":{"date-parts":[[2006,1,25]],"date-time":"2006-01-25T21:53:41Z","timestamp":1138226021000},"page":"439-444","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":8,"title":["Rifalazil Pretreatment of Mammalian Cell Cultures Prevents Subsequent Chlamydia Infection"],"prefix":"10.1128","volume":"50","author":[{"given":"Robert J.","family":"Suchland","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, University of Washington, Seattle, Washington 98195"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kara","family":"Brown","sequence":"additional","affiliation":[{"name":"ActivBiotics, Inc., Lexington, Massachusetts 02421"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David M.","family":"Rothstein","sequence":"additional","affiliation":[{"name":"ActivBiotics, Inc., Lexington, Massachusetts 02421"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Walter E.","family":"Stamm","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, University of Washington, Seattle, Washington 98195"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"1","volume":"47","year":"1998","unstructured":"Centers for Disease Control and Prevention. 1998. 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Expanding indications for the new macrolides, azalides, and streptogramins. Infect. Dis. Ther. Ser.21:317-321.","journal-title":"Infect. Dis. Ther. Ser."},{"key":"e_1_3_2_9_2","first-page":"903","volume":"49","year":"2005","unstructured":"Kutlin, A., S. Kohlhoff, P. Roblin, M. R. Hammerschlag, and P. Riska. 2005. Emergence of resistance to rifampin and rifalazil in Chlamydophila pneumoniae and Chlamydia trachomatis. Antimicrob. Agents Chemother. 200549:903-907.","journal-title":"Antimicrob. Agents Chemother. 2005"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1001\/archpedi.155.8.947"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.47.3.1135-1136.2003"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1517\/13543784.12.2.255"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(98)12387-5"},{"key":"e_1_3_2_14_2","unstructured":"Stamm W. E. W. M. Geisler and R. J. Suchland. 2002. Assessment of antimicrobial resistance in Chlamydia trachomatis strains associated with treatment failure or same strain recurrence p. 353-360. In Chlamydial infections: proceeding of the 105th International Symposium on Human Chlamydial Infections Antalya Turkey."},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.49.3.1120-1126.2005"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.47.2.636-642.2003"},{"key":"e_1_3_2_17_2","first-page":"117","volume":"26","year":"2001","unstructured":"Whittington, W. L., C. Kent, P. Kissinger, M. K. Oh, J. D. Fortenberry, S. E. Hillis, B. Litchfield, G. A. Bolan, M. E. St Louis, T. A. Farley, and H. H. Handsfield. 2001. Determinants of persistent and recurrent Chlamydia in young women: results of a multicenter cohort study. Sex. Transm. Dis.26:117-123.","journal-title":"Sex. Transm. 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