{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T15:57:21Z","timestamp":1787587041917,"version":"build-2736575974"},"reference-count":32,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2024,10,27]],"date-time":"2024-10-27T00:00:00Z","timestamp":1729987200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2024,10,27]],"date-time":"2024-10-27T00:00:00Z","timestamp":1729987200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100003710","name":"Korea Health Industry Development Institute","doi-asserted-by":"publisher","award":["HR21C0198"],"award-info":[{"award-number":["HR21C0198"]}],"id":[{"id":"10.13039\/501100003710","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2025,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Air pollutants, such as diesel exhaust particles (DEPs), induce respiratory disease exacerbation with neutrophilic infiltration. Progranulin (PGRN), an epithelial cell and macrophage\u2010derived secretory protein, is associated with neutrophilic inflammation. PGRN is digested into various derivatives at inflammatory sites and is involved in several inflammatory processes. PGRN and its derivatives likely regulate responses to DEP exposure in allergic airway inflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>To investigate the role of PGRN and its derivatives in the regulation of responses to DEP exposure in allergic airway inflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A murine model of allergic airway inflammation was generated in PGRN\u2010deficient mice, and they were simultaneously exposed to DEP followed by intranasal administration of full\u2010length recombinant PGRN (PGRN\u2010FL) and a PGRN\u2010derived fragment (FBAC). Inflammatory status was evaluated by bronchoalveolar lavage fluid and histopathologic analyses. Human bronchial epithelial cells were stimulated with DEPs and house dust mites (HDMs), and the effect of FBAC treatment was evaluated by assessing various intracellular signaling molecules, autophagy markers, inflammatory cytokines, and intracellular oxidative stress.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>DEP exposure exaggerated neutrophilic inflammation, enhanced IL\u20106 and CXCL15 secretions, and increased oxidative stress in the murine model; this effect was greater in PGRN\u2010deficient mice than in wild\u2010type mice. The DEP\u2010exposed mice with PGRN\u2010FL treatment revealed no change in neutrophil infiltration and higher oxidative stress status in the lungs. On the contrary, FBAC administration inhibited neutrophilic infiltration and reduced oxidative stress. In human bronchial epithelial cells, DEP and HDM exposure increased intracellular oxidative stress and IL\u20106 and IL\u20108 secretion. Decreased nuclear factor erythroid 2\u2010related factor 2 (Nrf2) expression and increased phosphor\u2010p62 and LC3B expression were also observed. FBAC treatment attenuated oxidative stress from DEP and HDM exposure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>FBAC reduced neutrophilic inflammation exaggerated by DEP exposure in a mouse model of allergic airway inflammation by reducing oxidative stress. PGRN and PGRN\u2010derived proteins may be novel therapeutic agents in attenuating asthma exacerbation induced by air pollutant exposure.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/all.16362","type":"journal-article","created":{"date-parts":[[2024,10,27]],"date-time":"2024-10-27T07:09:18Z","timestamp":1730012958000},"page":"703-714","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Progranulin derivative attenuates lung neutrophilic infiltration from diesel exhaust particle exposure"],"prefix":"10.1111","volume":"80","author":[{"given":"A. Ryang","family":"Lee","sequence":"first","affiliation":[{"name":"Division of Allergy and Clinical Immunology, Department of Internal Medicine, Asan Medical Center University of Ulsan College of Medicine  Seoul Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mini","family":"Jeong","sequence":"additional","affiliation":[{"name":"Division of Allergy and Clinical Immunology, Department of Internal Medicine, Asan Medical Center University of Ulsan College of Medicine  Seoul Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyomoon","family":"Koo","sequence":"additional","affiliation":[{"name":"Division of Allergy and Clinical Immunology, Department of Internal Medicine, Asan Medical Center University of Ulsan College of Medicine  Seoul Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sin\u2010Jeong","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Allergy and Clinical Immunology, Department of 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