{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T16:17:20Z","timestamp":1777393040329,"version":"3.51.4"},"reference-count":41,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2009,4,1]],"date-time":"2009-04-01T00:00:00Z","timestamp":1238544000000},"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":[[2009,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The gram-negative rod\n            <jats:italic>Burkholderia pseudomallei<\/jats:italic>\n            is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical areas. The bacterium multiplies intracellularly within the cytosol, induces the formation of actin tails, and can spread directly from cell to cell. Recently, it has been shown that\n            <jats:italic>B. pseudomallei<\/jats:italic>\n            can induce caspase-1-dependent cell death in macrophages. The aim of the present study was to further elucidate the role of caspase-1 during\n            <jats:italic>B. pseudomallei<\/jats:italic>\n            infection. In vivo experiments with\n            <jats:italic>caspase-1<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice revealed a high susceptibility to\n            <jats:italic>B. pseudomallei<\/jats:italic>\n            challenge. This phenotype was associated with a significantly higher bacterial burden 2 days after infection and decreased gamma interferon (IFN-\u03b3) and interleukin-18 cytokine levels 24 h after infection compared to control animals.\n            <jats:italic>caspase-1<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            bone marrow-derived macrophages (BMM) exhibited strong caspase-3 expression and reduced cell damage compared to wild-type (WT) cells during early\n            <jats:italic>B. pseudomallei<\/jats:italic>\n            infection, indicating \u201cclassical\u201d apoptosis, whereas WT BMM showed signs of rapid caspase-1-dependent cell death. Moreover, we found that\n            <jats:italic>caspase-1<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            BMM had a strongly increased bacterial burden compared to WT cells 3 h after infection under conditions where no difference in cell death could be observed between both cell populations at this time point. We therefore suggest that caspase-1-dependent rapid cell death might contribute to resistance by reducing the intracellular niche for\n            <jats:italic>B. pseudomallei<\/jats:italic>\n            , but, in addition, caspase-1 might also have a role in controlling intracellular replication of\n            <jats:italic>B. pseudomallei<\/jats:italic>\n            in macrophages. Moreover, caspase-1-dependent IFN-\u03b3 production is likely to contribute to resistance in murine melioidosis.\n          <\/jats:p>","DOI":"10.1128\/iai.01257-08","type":"journal-article","created":{"date-parts":[[2009,1,30]],"date-time":"2009-01-30T01:45:10Z","timestamp":1233279910000},"page":"1589-1595","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":35,"title":["Caspase-1 Mediates Resistance in Murine Melioidosis"],"prefix":"10.1128","volume":"77","author":[{"given":"Katrin","family":"Breitbach","sequence":"first","affiliation":[{"name":"Friedrich Loeffler Institute of Medical Microbiology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guang Wen","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, National University of Singapore, Singapore, Republic of Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jens","family":"Ko\u0308hler","sequence":"additional","affiliation":[{"name":"Friedrich Loeffler Institute of Medical Microbiology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kristin","family":"Eske","sequence":"additional","affiliation":[{"name":"Friedrich Loeffler Institute of Medical Microbiology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patimaporn","family":"Wongprompitak","sequence":"additional","affiliation":[{"name":"Friedrich Loeffler Institute of Medical Microbiology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany"},{"name":"Department of Immunology, Faculty of Medicine Siriraj, Mahidol University, Bangkok, Thailand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gladys","family":"Tan","sequence":"additional","affiliation":[{"name":"Defence Medical and Environmental Research Institute, DSO National Laboratories, Singapore, Republic of Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yichun","family":"Liu","sequence":"additional","affiliation":[{"name":"Defence Medical and Environmental Research Institute, DSO National Laboratories, Singapore, Republic of Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yunn-Hwen","family":"Gan","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, National University of Singapore, Singapore, Republic of Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ivo","family":"Steinmetz","sequence":"additional","affiliation":[{"name":"Friedrich Loeffler Institute of Medical Microbiology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M604933200"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-695X.2008.00389.x"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00966-06"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1462-5822.2003.00277.x"},{"key":"e_1_3_2_6_2","first-page":"41","volume":"10","year":"2008","unstructured":"Cervantes, J., T. 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