{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T05:20:55Z","timestamp":1787721655022,"version":"build-2784847793"},"reference-count":91,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T00:00:00Z","timestamp":1787702400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Chronic pulmonary diseases, including cystic fibrosis, chronic obstructive pulmonary disease, and chronic bronchitis, as well as ventilator-associated pneumonia, are characterized by persistent infection of mucus-laden airways.\n                    <jats:italic>Pseudomonas aeruginosa<\/jats:italic>\n                    (PA) is a dominant pathogen in these conditions and produces volatile organic compounds (VOCs) that have been proposed as biomarkers of disease exacerbation; however, their immunopathogenic roles remain unclear. We investigated PA-derived VOCs using human bronchial epithelial air\u2013liquid interface cultures and murine models. VOCs exposure significantly increased airway mucin expression and induced a proinflammatory response characterized by M1 macrophage polarization (iNOS\n                    <jats:sup>+<\/jats:sup>\n                    ), neutrophil recruitment, and expansion of IL-17A\u2013producing Thy1.2\n                    <jats:sup>+<\/jats:sup>\n                    lymphocytes. Functional depletion of macrophages, neutrophils, or IL-17A\n                    <jats:italic>in vivo<\/jats:italic>\n                    each attenuated mucin production and goblet cell metaplasia, indicating non-redundant contributions to mucus pathology.\n                    <jats:italic>In vitro<\/jats:italic>\n                    , IL-17A neutralization partially restored FOXA2 expression and reduced mucin production, supporting a role in mucus regulation. On the mechanistic level, we discovered an IL-17A-dependent dual-axis pathway involving both epithelial cell-mediated autocrine and lymphocyte-mediated paracrine signaling that contributes to the feed-forward loop of inflammation and enhances the signaling pathways regulating mucus hypersecretion in airways. We conclude that PA VOCs activate multiple proinflammatory responses to convergently drive mucus pathogenesis in the diseased lung.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1823251","type":"journal-article","created":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T04:50:42Z","timestamp":1787719842000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Pseudomonas aeruginosa-derived volatile organic compounds modulate host immunity to disrupt airway mucus homeostasis"],"prefix":"10.3389","volume":"17","author":[{"given":"Shanny Hsuan","family":"Kuo","sequence":"first","affiliation":[{"name":"Department of Pathobiology, College of Veterinary Medicine, University of Illinois Urbana-Champaign","place":["Urbana, IL, United States"]},{"name":"Department of Comparative Medicine, School of Medicine, University of Washington","place":["Seattle, WA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaishree","family":"Sharma","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, College of Veterinary Medicine, University of Illinois Urbana-Champaign","place":["Urbana, IL, United States"]},{"name":"Fred Hutchinson Cancer Center","place":["Seattle, WA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cong","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, College of Veterinary Medicine, University of Illinois Urbana-Champaign","place":["Urbana, IL, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miranda D.","family":"Vieson","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, College of Veterinary Medicine, University of Illinois Urbana-Champaign","place":["Urbana, IL, United States"]},{"name":"Veterinary Diagnostic Laboratory, College of Veterinary Medicine, University of Illinois Urbana-Champaign","place":["Urbana, IL, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beata","family":"Kosmider","sequence":"additional","affiliation":[{"name":"Center for Inflammation and Lung Research, Department of Microbiology, Immunology and Inflammation, Lewis Katz School of Medicine, Temple University","place":["Philadelphia, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Scott H.","family":"Randell","sequence":"additional","affiliation":[{"name":"Marsico Lung Institute\/Cystic Fibrosis Center, School of Medicine, University of North Carolina at Chapel Hill","place":["Chapel Hill, NC, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Som G.","family":"Nanjappa","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, College of Veterinary Medicine, University of Illinois Urbana-Champaign","place":["Urbana, IL, United 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