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To gain insight into the mechanisms by which<jats:italic>C. burnetii<\/jats:italic>is able to multiply intracellularly, we examined the ability of host cells to respond to signals that normally induce apoptosis. Our data show that mammalian cells infected with<jats:italic>C. burnetii<\/jats:italic>are resistant to apoptosis induced by staurosporine and UV light.<jats:italic>C. burnetii<\/jats:italic>infection prevented caspase 3\/7 activation and limited fragmentation of the host cell nucleus in response to agonists that induce apoptosis. Inhibition of bacterial protein synthesis reduced the antiapoptotic effect that<jats:italic>C. burnetii<\/jats:italic>exerted on infected host cells. Inhibition of apoptosis in<jats:italic>C. burnetii<\/jats:italic>-infected cells did not correlate with the degradation of proapoptotic BH3-only proteins involved in activation of the intrinsic cell death pathway; however, cytochrome<jats:italic>c<\/jats:italic>release from mitochondria was diminished in cells infected with<jats:italic>C. burnetii<\/jats:italic>upon induction of apoptosis. These data indicate that<jats:italic>C. burnetii<\/jats:italic>can interfere with the intrinsic cell death pathway during infection by producing proteins that either directly or indirectly prevent release of cytochrome<jats:italic>c<\/jats:italic>from mitochondria. It is likely that inhibition of apoptosis by<jats:italic>C. burnetii<\/jats:italic>represents an important virulence property that allows this obligate intracellular pathogen to maintain host cell viability despite inducing stress that would normally activate the intrinsic death pathway.<\/jats:p>","DOI":"10.1128\/iai.00863-07","type":"journal-article","created":{"date-parts":[[2007,8,21]],"date-time":"2007-08-21T00:58:49Z","timestamp":1187657929000},"page":"5282-5289","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":101,"title":["<i>Coxiella burnetii<\/i>Inhibits Activation of Host Cell Apoptosis through a Mechanism That Involves Preventing Cytochrome<i>c<\/i>Release from Mitochondria"],"prefix":"10.1128","volume":"75","author":[{"given":"Anja","family":"Lu\u0308hrmann","sequence":"first","affiliation":[{"name":"Yale University School of Medicine, Section of Microbial Pathogenesis, 295 Congress Avenue, New Haven, Connecticut 06536"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Craig R.","family":"Roy","sequence":"additional","affiliation":[{"name":"Yale University School of Medicine, Section of Microbial Pathogenesis, 295 Congress Avenue, New Haven, Connecticut 06536"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-5822.2006.00785.x"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(02)00381-2"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.40.3.1155-1162.1983"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/0966-842X(94)90651-3"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/mr.47.2.127-149.1983"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0611030104"},{"key":"e_1_3_2_8_2","first-page":"98","volume":"69","year":"1956","unstructured":"Benenson, A. 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