{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T01:15:28Z","timestamp":1788225328366,"version":"build-2803163510"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T00:00:00Z","timestamp":1770076800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T00:00:00Z","timestamp":1770076800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2026,2,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Dermatophagoides farinae<\/jats:italic>\n                      (DFA), the most prevalent aeroallergen in allergic asthma, releases extracellular vesicles (EVs) containing dfa-miR-276-3p, which plays an important role in DFA sensitization. In this study, we utilized AAV-dfa-miR-276-3p to create a mouse model with dfa-miR-276-3p overexpression in lungs. Using this model, we demonstrated that dfa-miR-276-3p acted as a priming factor that exacerbated DFA extract (DFE)-induced airway inflammation in mice. We also confirmed that dfa-miR-276-3p functioned as a priming pro-inflammatory factor in human bronchial epithelial BEAS-2B cells, enhancing the release of inflammatory cytokines induced by DFE. Furthermore, we found that dfa-miR-276-3p regulated stanniocalcin 1 (STC1) in a targeted manner, leading to increased inflammatory cytokine secretion and activation of the reactive oxygen species (ROS)\/nuclear factor kappa B (NF-\u03baB) pathway. Notably, the addition of recombinant human STC1 alleviated the inflammatory effects of dfa-miR-276-3p, reducing airway inflammation and dampening ROS\/NF-\u03baB signaling. Parallel findings in mouse models confirmed that dfa-miR-276-3p drove DFA-induced airway inflammation through STC1-dependent regulation of the ROS\/NF-\u03baB pathway. Our study reveals a cross-kingdom regulatory role for DFA-derived miRNAs in the pathogenesis of allergic asthma, highlighting dfa-miR-276-3p as a crucial priming factor in the process of allergic airway inflammation induced by DFA.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        We demonstrated that dfa-miR-276-3p acted as a priming factor that exacerbated\n                        <jats:italic toggle=\"yes\">Dermatophagoides farinae<\/jats:italic>\n                        (DFA) extract-induced airway inflammation in mice, and functioned as a priming pro-inflammatory factor in human bronchial epithelial BEAS-2B cells. In addition, dfa-miR-276-3p was found to regulate stanniocalcin 1 (STC1) in a targeted manner, leading to increased secretion of inflammatory cytokines and activation of the reactive oxygen species (ROS)\/nuclear factor kappa B (NF-\u03baB) pathway, and addition of recombinant human STC1 alleviated the inflammatory effects of dfa-miR-276-3p, reducing airway inflammation and dampening ROS\/NF-\u03baB signaling. Parallel findings in mouse models confirmed that dfa-miR-276-3p drove DFA-induced airway inflammation through STC1-dependent regulation of the ROS\/NF-\u03baB pathway. Our findings provide new insights into the role of DFA-derived miRNAs in the development of allergic asthma and propose an alternative pathway for DFA sensitization that may have significant clinical implications for allergy prevention and treatment.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/spectrum.01923-25","type":"journal-article","created":{"date-parts":[[2025,12,22]],"date-time":"2025-12-22T14:04:39Z","timestamp":1766412279000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["A novel role of\n                    <i>Dermatophagoides farinae<\/i>\n                    -derived miR-276-3p in aggravating mite-induced allergic airway inflammation"],"prefix":"10.1128","volume":"14","author":[{"given":"Xiao","family":"Zang","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/059gcgy73","id-type":"ROR","asserted-by":"publisher"}],"name":"School of Public Health, Nanjing Medical University","place":["Nanjing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shangde","family":"Jiang","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/059gcgy73","id-type":"ROR","asserted-by":"publisher"}],"name":"School of Public Health, Nanjing Medical University","place":["Nanjing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinyan","family":"Yu","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/059gcgy73","id-type":"ROR","asserted-by":"publisher"}],"name":"School of Clinical Laboratory Medicine, Nanjing Medical University","place":["Nanjing, 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