{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T07:05:37Z","timestamp":1790406337135,"version":"4.1.0"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2016,5,1]],"date-time":"2016-05-01T00:00:00Z","timestamp":1462060800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI087669"],"award-info":[{"award-number":["R01AI087669"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R21AI107148"],"award-info":[{"award-number":["R21AI107148"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"HHS | NIH | National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["P20GM103625"],"award-info":[{"award-number":["P20GM103625"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"HHS | NIH | National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1TR000039"],"award-info":[{"award-number":["UL1TR000039"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008231","name":"Arkansas Biosciences Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008231","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2016,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:named-content content-type=\"genus-species\">Coxiella burnetii<\/jats:named-content>\n                    is an intracellular bacterial pathogen that causes human Q fever, an acute debilitating flu-like illness that can also present as chronic endocarditis. Disease typically occurs following inhalation of contaminated aerosols, resulting in an initial pulmonary infection. In human cells,\n                    <jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>\n                    generates a replication niche termed the parasitophorous vacuole (PV) by directing fusion with autophagosomes and lysosomes.\n                    <jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>\n                    requires this lysosomal environment for replication and uses a Dot\/Icm type IV secretion system to generate the large PV. However, we do not understand how\n                    <jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>\n                    evades the intracellular immune surveillance that triggers an inflammatory response. We recently characterized human alveolar macrophage (hAM) infection\n                    <jats:italic>in vitro<\/jats:italic>\n                    and found that avirulent\n                    <jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>\n                    triggers sustained interleukin-1\u03b2 (IL-1\u03b2) production. Here, we evaluated infection of\n                    <jats:italic>ex vivo<\/jats:italic>\n                    human lung tissue, defining a valuable approach for characterizing\n                    <jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>\n                    interactions with a human host. Within whole lung tissue,\n                    <jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>\n                    preferentially replicated in hAMs. Additionally, IL-1\u03b2 production correlated with formation of an apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC)-dependent inflammasome in response to infection. We also assessed potential activation of a human-specific noncanonical inflammasome and found that caspase-4 and caspase-5 are processed during infection. Interestingly, although inflammasome activation is closely linked to pyroptosis, lytic cell death did not occur following\n                    <jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>\n                    -triggered inflammasome activation, indicating an atypical response after intracellular detection. Together, these studies provide a novel platform for studying the human innate immune response to\n                    <jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>\n                    .\n                  <\/jats:p>","DOI":"10.1128\/iai.00012-16","type":"journal-article","created":{"date-parts":[[2016,2,22]],"date-time":"2016-02-22T22:43:26Z","timestamp":1456181006000},"page":"1438-1445","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":38,"title":["Development of an\n                    <i>Ex Vivo<\/i>\n                    Tissue Platform To Study the Human Lung Response to Coxiella burnetii"],"prefix":"10.1128","volume":"84","author":[{"given":"Joseph G.","family":"Graham","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, 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