{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T18:03:51Z","timestamp":1790618631356,"version":"4.1.0"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2018,1,1]],"date-time":"2018-01-01T00:00:00Z","timestamp":1514764800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,1,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Immunity against microbes depends on recognition of pathogen-associated molecular patterns by innate receptors. Signaling pathways triggered by Brucella abortus DNA involves TLR9, AIM2, and stimulator of IFN genes (STING). In this study, we observed by microarray analysis that several type I IFN\u2013associated genes, such as IFN-\u03b2 and guanylate-binding proteins (GBPs), are downregulated in STING knockout (KO) macrophages infected with Brucella or transfected with DNA. Additionally, we determined that STING and cyclic GMP\u2013AMP synthase (cGAS) are important to engage the type I IFN pathway, but only STING is required to induce IL-1\u03b2 secretion, caspase-1 activation, and GBP2 and GBP3 expression. Furthermore, we determined that STING but not cGAS is critical for host protection against Brucella infection in macrophages and in vivo. This study provides evidence of a cGAS-independent mechanism of STING-mediated protection against an intracellular bacterial infection. Additionally, infected IFN regulatory factor-1 and IFNAR KO macrophages had reduced GBP2 and GBP3 expression and these cells were more permissive to Brucella replication compared with wild-type control macrophages. Because GBPs are critical to target vacuolar bacteria, we determined whether GBP2 and GBPchr3 affect Brucella control in vivo. GBPchr3 but not GBP2 KO mice were more susceptible to bacterial infection, and small interfering RNA treated\u2013macrophages showed reduction in IL-1\u03b2 secretion and caspase-1 activation. Finally, we also demonstrated that Brucella DNA colocalizes with AIM2, and AIM2 KO mice are less resistant to B. abortus infection. In conclusion, these findings suggest that the STING-dependent type I IFN pathway is critical for the GBP-mediated release of Brucella DNA into the cytosol and subsequent activation of AIM2.<\/jats:p>","DOI":"10.4049\/jimmunol.1700725","type":"journal-article","created":{"date-parts":[[2017,12,4]],"date-time":"2017-12-04T17:10:22Z","timestamp":1512407422000},"page":"607-622","source":"Crossref","is-referenced-by-count":112,"title":["<i>Brucella abortus<\/i> Triggers a cGAS-Independent STING Pathway To Induce Host Protection That Involves Guanylate-Binding Proteins and Inflammasome Activation"],"prefix":"10.1093","volume":"200","author":[{"given":"Miriam M","family":"Costa Franco","sequence":"first","affiliation":[{"name":"Departamento de Bioquimica e Imunologia, Universidade Federal de Minas Gerais , Belo Horizonte, 31270-901 Minas 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Minas Gerais,","place":["Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8051-3396","authenticated-orcid":false,"given":"Daiane M","family":"Cerqueira","sequence":"additional","affiliation":[{"name":"Departamento de Bioquimica e Imunologia, Universidade Federal de Minas Gerais , Belo Horizonte, 31270-901 Minas Gerais,","place":["Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7627-3000","authenticated-orcid":false,"given":"Juliana","family":"Alves-Silva","sequence":"additional","affiliation":[{"name":"Departamento de Bioquimica e Imunologia, Universidade Federal de Minas Gerais , Belo Horizonte, 31270-901 Minas Gerais,","place":["Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1343-0977","authenticated-orcid":false,"given":"Jerome","family":"Harms","sequence":"additional","affiliation":[{"name":"Department of 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