{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T02:18:55Z","timestamp":1785291535060,"version":"3.55.0"},"update-to":[{"DOI":"10.1371\/journal.ppat.1009020","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2020,11,6]],"date-time":"2020-11-06T00:00:00Z","timestamp":1604620800000}}],"reference-count":68,"publisher":"Public Library of Science (PLoS)","issue":"10","license":[{"start":{"date-parts":[[2020,10,27]],"date-time":"2020-10-27T00:00:00Z","timestamp":1603756800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>Brucellosis, caused by a number of <jats:italic>Brucella<\/jats:italic> species, remains the most prevalent zoonotic disease worldwide. <jats:italic>Brucella<\/jats:italic> establish chronic infections within host macrophages despite triggering cytosolic innate immune sensors, including Stimulator of Interferon Genes (STING), which potentially limit infection. In this study, STING was required for control of chronic <jats:italic>Brucella<\/jats:italic> infection <jats:italic>in vivo<\/jats:italic>. However, early during infection, <jats:italic>Brucella<\/jats:italic> down-regulated STING mRNA and protein. Down-regulation occurred post-transcriptionally, required live bacteria, the <jats:italic>Brucella<\/jats:italic> type IV secretion system, and was independent of host IRE1-RNase activity. STING suppression occurred in <jats:italic>MyD88<\/jats:italic>-\/- macrophages and was not induced by Toll-like receptor agonists or purified <jats:italic>Brucella<\/jats:italic> lipopolysaccharide (LPS). Rather, <jats:italic>Brucella<\/jats:italic> induced a STING-targeting microRNA, miR-24-2, in a type IV secretion system-dependent manner. Furthermore, STING downregulation was inhibited by miR-24 anti-miRs and in <jats:italic>Mirn23a<\/jats:italic> locus-deficient macrophages. Failure to suppress STING expression in <jats:italic>Mirn23a<\/jats:italic><jats:sup>-\/-<\/jats:sup> macrophages correlated with diminished <jats:italic>Brucella<\/jats:italic> replication, and was rescued by exogenous miR-24. <jats:italic>Mirn23a<\/jats:italic>-\/- mice were also more resistant to splenic colonization one week post infection. Anti-miR-24 potently suppressed replication in wild type, but much less in STING<jats:sup>-\/-<\/jats:sup> macrophages, suggesting most of the impact of miR-24 induction on replication occurred via STING suppression. In summary, <jats:italic>Brucella<\/jats:italic> sabotages cytosolic surveillance by miR-24-dependent suppression of STING expression; post-STING activation \u201cdamage control\u201d via targeted STING destruction may enable establishment of chronic infection.<\/jats:p>","DOI":"10.1371\/journal.ppat.1009020","type":"journal-article","created":{"date-parts":[[2020,10,27]],"date-time":"2020-10-27T17:51:56Z","timestamp":1603821116000},"page":"e1009020","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":30,"title":["Brucella suppress STING expression via miR-24 to enhance infection"],"prefix":"10.1371","volume":"16","author":[{"given":"Mike","family":"Khan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jerome 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