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Type I IFN supports host protection from a related pathogen,<jats:named-content content-type=\"genus-species\">Legionella pneumophila<\/jats:named-content>, and we hypothesized that it would be similarly protective in<jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>infection. In contrast to our prediction, IFN-\u03b1 receptor-deficient (IFNAR<jats:sup>\u2212\/\u2212<\/jats:sup>) mice were protected from<jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>-induced infection. Therefore, the role of type I IFN in<jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>infection was distinct from that in<jats:named-content content-type=\"genus-species\">L. pneumophila<\/jats:named-content>. Mice treated with a double-stranded-RNA mimetic were protected from<jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>-induced weight loss through an IFNAR-independent pathway. We next treated mice with recombinant IFN-\u03b1 (rIFN-\u03b1). When rIFN-\u03b1 was injected by the intraperitoneal route during infection, disease-induced weight loss was exacerbated. Mice that received rIFN-\u03b1 by this route had dampened interleukin 1\u03b2 (IL-1\u03b2) expression in bronchoalveolar lavage fluids. However, when rIFN-\u03b1 was delivered to the lung, bacterial replication was decreased in all tissues. Thus, the presence of type I IFN in the lung protected from infection, but when delivered to the periphery, type I IFN enhanced disease, potentially by dampening inflammatory cytokines. To better characterize the capacity for type I IFN induction by<jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>, we assessed expression of IFN-\u03b2 transcripts by human macrophages following stimulation with lipopolysaccharide (LPS) from<jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>. Understanding innate responses in<jats:named-content content-type=\"genus-species\">C. burnetii<\/jats:named-content>infection will support the discovery of novel therapies that may be alternative or complementary to the current antibiotic treatment.<\/jats:p>","DOI":"10.1128\/iai.01540-15","type":"journal-article","created":{"date-parts":[[2016,4,12]],"date-time":"2016-04-12T03:23:49Z","timestamp":1460431429000},"page":"1815-1825","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":21,"title":["Type I Interferon Counters or Promotes Coxiella burnetii Replication Dependent on Tissue"],"prefix":"10.1128","volume":"84","author":[{"given":"Jodi F.","family":"Hedges","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University, Bozeman, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amanda","family":"Robison","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University, Bozeman, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily","family":"Kimmel","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University, Bozeman, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly","family":"Christensen","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University, Bozeman, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin","family":"Lucas","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University, Bozeman, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Ramstead","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University, Bozeman, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark A.","family":"Jutila","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University, Bozeman, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20040712"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature13489"},{"key":"e_1_3_2_4_2","first-page":"1931","article-title":"Staphylococcus aureus activates type I IFN signaling in mice and humans through the Xr repeated sequences of protein A","volume":"119","author":"Martin FJ","year":"2009","unstructured":"Martin FJ, Gomez MI, Wetzel DM, Memmi G, O'Seaghdha M, Soong G, Schindler C, Prince A. 2009. 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