{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T07:40:43Z","timestamp":1791272443718,"version":"4.1.0"},"reference-count":68,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2013,2,1]],"date-time":"2013-02-01T00:00:00Z","timestamp":1359676800000},"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":["Eukaryot Cell"],"published-print":{"date-parts":[[2013,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The prokaryote\n            <jats:named-content content-type=\"genus-species\">Chlamydia trachomatis<\/jats:named-content>\n            and the protozoan\n            <jats:named-content content-type=\"genus-species\">Toxoplasma gondii<\/jats:named-content>\n            , two obligate intracellular pathogens of humans, have evolved a similar\n            <jats:named-content content-type=\"genus-species\">modus operandi<\/jats:named-content>\n            to colonize their host cell and salvage nutrients from organelles. In order to gain fundamental knowledge on the pathogenicity of these microorganisms, we have established a cell culture model whereby single fibroblasts are coinfected by\n            <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n            and\n            <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n            . We previously reported that the two pathogens compete for the same nutrient pools in coinfected cells and that\n            <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n            holds a significant competitive advantage over\n            <jats:named-content content-type=\"genus-species\">Chlamydia<\/jats:named-content>\n            . Here we have expanded our coinfection studies by examining the respective abilities of\n            <jats:named-content content-type=\"genus-species\">Chlamydia<\/jats:named-content>\n            and\n            <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n            to co-opt the host cytoskeleton and recruit organelles. We demonstrate that the two pathogen-containing vacuoles migrate independently to the host perinuclear region and rearrange the host microtubular network around each vacuole. However,\n            <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n            outcompetes\n            <jats:named-content content-type=\"genus-species\">Chlamydia<\/jats:named-content>\n            to the host microtubule-organizing center to the detriment of the bacterium, which then shifts to a stress-induced persistent state. Solely in cells preinfected with\n            <jats:named-content content-type=\"genus-species\">Chlamydia<\/jats:named-content>\n            , the centrosomes become associated with the chlamydial inclusion, while the\n            <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n            parasitophorous vacuole displays growth defects. Both pathogens fragment the host Golgi apparatus and recruit Golgi elements to retrieve sphingolipids. This study demonstrates that the productive infection by both\n            <jats:named-content content-type=\"genus-species\">Chlamydia<\/jats:named-content>\n            and\n            <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n            depends on the capability of each pathogen to successfully adhere to a finely tuned developmental program that aims to remodel the host cell for the pathogen's benefit. In particular, this investigation emphasizes the essentiality of host organelle interception by intravacuolar pathogens to facilitate access to nutrients.\n          <\/jats:p>","DOI":"10.1128\/ec.00313-12","type":"journal-article","created":{"date-parts":[[2012,12,16]],"date-time":"2012-12-16T02:04:45Z","timestamp":1355623485000},"page":"265-277","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":18,"title":["Fierce Competition between Toxoplasma and Chlamydia for Host Cell Structures in Dually Infected Cells"],"prefix":"10.1128","volume":"12","author":[{"given":"Julia D.","family":"Romano","sequence":"first","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine","family":"de Beaumont","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jose A.","family":"Carrasco","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen","family":"Ehrenman","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrik M.","family":"Bavoil","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isabelle","family":"Coppens","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.chom.2009.05.014"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.micro.61.080706.093305"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1101\/gr.3724205"},{"key":"e_1_3_2_5_2","first-page":"139","volume-title":"Chlamydia: intracellular biology, pathogenesis, and immunity","author":"Schachter J","year":"1999","unstructured":"SchachterJ. 1999. 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