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Human stimulator of interferon genes (STING) induces an innate immune response through the induction of type I interferons (IFNs), and IFN promotes or suppresses\n              <jats:italic>C. burnetii<\/jats:italic>\n              replication, depending on tissue type.\n              <jats:italic>Drosophila melanogaster<\/jats:italic>\n              contains a functional STING ortholog (Sting) which activates NF-\u03baB signaling and autophagy. Here, we sought to address the role of\n              <jats:italic>D. melanogaster<\/jats:italic>\n              Sting during\n              <jats:italic>C. burnetii<\/jats:italic>\n              infection to uncover how Sting regulates\n              <jats:italic>C. burnetii<\/jats:italic>\n              infection in flies. We show that Sting-null flies exhibit higher mortality and reduced induction of antimicrobial peptides following\n              <jats:italic>C. burnetii<\/jats:italic>\n              infection compared to control flies. Additionally\n              <jats:italic>,<\/jats:italic>\n              Sting-null flies induce lower levels of oxidative stress genes during infection, but the provision of N-acetyl-cysteine (NAC) in food rescues Sting-null host survival. Lastly, we find that reactive oxygen species levels during\n              <jats:italic>C. burnetii<\/jats:italic>\n              infection are higher in\n              <jats:italic>Drosophila<\/jats:italic>\n              S2 cells knocked down for Sting compared to control cells. Our results show that at the host level, NAC provides protection against\n              <jats:italic>C. burnetii<\/jats:italic>\n              infection in the absence of Sting, thus establishing a role for Sting in protection against oxidative stress during\n              <jats:italic>C. burnetii<\/jats:italic>\n              infection.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/iai.00560-22","type":"journal-article","created":{"date-parts":[[2024,2,16]],"date-time":"2024-02-16T14:00:34Z","timestamp":1708092034000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":5,"title":["<i>Drosophila melanogaster<\/i>\n            Sting mediates\n            <i>Coxiella burnetii<\/i>\n            infection by reducing accumulation of reactive oxygen species"],"prefix":"10.1128","volume":"92","author":[{"given":"Rosa M.","family":"Guzman","sequence":"first","affiliation":[{"name":"School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathan G.","family":"Savolainen","sequence":"additional","affiliation":[{"name":"School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivia M.","family":"Hayden","sequence":"additional","affiliation":[{"name":"School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miyoung","family":"Lee","sequence":"additional","affiliation":[{"name":"School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chelsea A.","family":"Osbron","sequence":"additional","affiliation":[{"name":"School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziying","family":"Liu","sequence":"additional","affiliation":[{"name":"School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Yang","sequence":"additional","affiliation":[{"name":"Paul G. 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