{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T02:09:25Z","timestamp":1768010965812,"version":"3.49.0"},"reference-count":59,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2007,6,1]],"date-time":"2007-06-01T00:00:00Z","timestamp":1180656000000},"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":[[2007,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The respiratory pathogen\n            <jats:italic>Chlamydia<\/jats:italic>\n            (\n            <jats:italic>Chlamydophila<\/jats:italic>\n            )\n            <jats:italic>pneumoniae<\/jats:italic>\n            is associated with chronic diseases, including atherosclerosis and giant-cell arteritis, which are accompanied by the occurrence of these obligate intracellular bacteria in blood vessels. There,\n            <jats:italic>C. pneumoniae<\/jats:italic>\n            seems to be present in a persistent state. Persistence is characterized by modified bacterial metabolism and morphology, as well as a reversible arrest of chlamydial development. In cell culture, this persistent state can be induced by gamma interferon (IFN-\u03b3). To elucidate this long-term interaction between chlamydiae and their host cells, microarray screening on epithelial HeLa cells was performed. Transcription of persistently (and productively) infected cells was compared with that of mock-infected cells. Sixty-six host cell genes were regulated at 24 h and\/or 96 h of IFN-\u03b3-induced persistence. Subsequently, a set of 17 human host cell genes related to apoptosis, cell cycle, or metabolism was identified as permanently up- or down-regulated by real-time PCR. Some of these chlamydia-dependent host cell responses were diminished or even absent in the presence of rifampin. However, other expression patterns were not altered by the inhibition of bacterial RNA polymerase, suggesting two different modes of host cell activation. Thus, in the IFN-\u03b3 model, the persisting bacteria cause long-lasting changes in the expression of genes coding for functionally important proteins. They might be potential drug targets for the treatment of persistent\n            <jats:italic>C. pneumoniae<\/jats:italic>\n            infections.\n          <\/jats:p>","DOI":"10.1128\/iai.01045-06","type":"journal-article","created":{"date-parts":[[2007,3,13]],"date-time":"2007-03-13T05:34:26Z","timestamp":1173764066000},"page":"2853-2863","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Host Cell Responses to\n            <i>Chlamydia pneumoniae<\/i>\n            in Gamma Interferon-Induced Persistence Overlap Those of Productive Infection and Are Linked to Genes Involved in Apoptosis, Cell Cycle, and Metabolism"],"prefix":"10.1128","volume":"75","author":[{"given":"Meike","family":"Eickhoff","sequence":"first","affiliation":[{"name":"Department of Research and Development, QIAGEN Hamburg GmbH, Koenigstrasse 4a, 22767 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jessica","family":"Thalmann","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Medical School Hannover, 30625 Hannover, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simone","family":"Hess","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, 10117 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Myriam","family":"Martin","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Medical School Hannover, 30625 Hannover, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Laue","sequence":"additional","affiliation":[{"name":"Department of Research and Development, QIAGEN Hamburg GmbH, Koenigstrasse 4a, 22767 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joachim","family":"Kruppa","sequence":"additional","affiliation":[{"name":"Center of Experimental Medicine, Institute of Molecular Cell Biology, University Hospital of Hamburg-Eppendorf, Martinistra\u00dfe 52, 20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gudrun","family":"Brandes","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Center of Anatomy, Medical School Hannover, 30625 Hannover, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andreas","family":"Klos","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Medical School Hannover, 30625 Hannover, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.573899"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/mr.58.4.686-699.1994"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3476(05)81812-8"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1515\/BC.2002.027"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.16.5556-5571.2003"},{"key":"e_1_3_2_7_2","unstructured":"J. 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