{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T21:20:58Z","timestamp":1790198458085,"version":"4.1.0"},"reference-count":48,"publisher":"Public Library of Science (PLoS)","issue":"3","license":[{"start":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T00:00:00Z","timestamp":1774569600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS One"],"abstract":"<jats:sec id=\"sec001\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Inflammatory bowel disease (IBD), a chronic inflammation of the gastrointestinal tract, is well recognized for triggering extraintestinal manifestations, including pulmonary complications. Emerging evidence highlights the\n                      <jats:italic>gut lung axis<\/jats:italic>\n                      (GLA) as a critical link in respiratory health, where gut dysbiosis and bacterial translocation play a role in systemic and pulmonary inflammation. Despite its clinical relevance, the mechanisms underlying these pulmonary manifestations remain poorly understood. The Stimulator of Interferon Genes (STING) pathway plays a critical role in regulating pulmonary inflammation. However, its precise role in colitis-associated lung inflammation remains unclear and could provide novel insights into the pathogenesis of this condition.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec002\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This study evaluates the involvement of STING pathway in colitis induced lung tissue inflammation using a dextran sulfate sodium (DSS) murine model of colitis. The effect of STING inhibitor on regulating steroid hypo-responsiveness, particularly the glucocorticoid receptor GR-\u03b1\/GR-\u03b2 ratio, is also examined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec003\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The DSS model induces lung inflammation, characterized by enhanced infiltration of inflammatory cells into lung tissues, increased levels of IL-17, IFN-\u03b3, bacterial DNA, while enhancing steroid hypo-responsiveness. The inhibition of STING controls lung inflammation and restores steroid sensitivity to a much higher extent compared to dexamethasone treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec004\">\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The significant activation of the STING pathway and dysregulation of steroid signature markers in the lungs of DSS-induced colitis mice suggest a novel mechanism by which gut inflammation may propagate to the lungs.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1371\/journal.pone.0344511","type":"journal-article","created":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T17:37:12Z","timestamp":1774633032000},"page":"e0344511","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":2,"title":["STING pathway contributes to Steroid-Hyporesponsive Lung Inflammation in DSS-induced colitis mice 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