{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T06:59:40Z","timestamp":1790405980032,"version":"4.1.0"},"reference-count":28,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T00:00:00Z","timestamp":1790294400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T00:00:00Z","timestamp":1790294400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Pediatric Discovery"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Airway epithelial cells contribute critically to the initiation of allergic airway inflammation via the release of alarmins such as interleukin\u201033 (IL\u201033). Nevertheless, the intracellular regulatory networks governing epithelial alarmin release remain inadequately defined. Although autophagy has been implicated in epithelial stress adaptation and the transcription factor early growth response 1 (\n                    <jats:italic>EGR1<\/jats:italic>\n                    ) is promptly induced upon allergen challenge, it remains uncertain whether\n                    <jats:italic>EGR1<\/jats:italic>\n                    contributes to IL\u201033 release as a representative indicator of epithelial activation through autophagy\u2010associated processes. In this study, human bronchial epithelial BEAS\u20102B cells were exposed to house dust mite (HDM) extract.\n                    <jats:italic>EGR1<\/jats:italic>\n                    expression was manipulated using gain\u2010 and loss\u2010of\u2010function strategies. Autophagy\u2010associated alterations were evaluated by monitoring LC3B, p62, and PI3K\u2010III (Vps34) levels, together with immunofluorescence microscopy. IL\u201033 release into culture supernatants was quantified by ELISA as a functional readout of\u00a0epithelial activation. Pharmacological interference with autophagy was employed to examine functional engagement. An HDM\u2010driven murine model was utilized to assess in vivo correlates. Publicly accessible transcriptomic datasets were interrogated in an exploratory manner to characterize epithelial stress signatures linked to this axis. HDM treatment upregulated\n                    <jats:italic>EGR1<\/jats:italic>\n                    in airway epithelial cells, concomitant with autophagy\u2010associated alterations and enhanced IL\u201033 release. Forced\n                    <jats:italic>EGR1<\/jats:italic>\n                    expression coincided with elevated LC3B\u2010II levels, diminished p62 accumulation, and increased PI3K\u2010III abundance, whereas\n                    <jats:italic>EGR1<\/jats:italic>\n                    silencing produced reciprocal effects. Pharmacological suppression of autophagy attenuated IL\u201033 release and inhibition of Class III PI3K blunted the\n                    <jats:italic>EGR1<\/jats:italic>\n                    overexpression\u2010driven increase in IL\u201033 release. In HDM\u2010challenged mice, colocalization of EGR1 and LC3B was observed in lung tissue sections. Exploratory transcriptomic profiling further suggested that allergen provocation may elicit a coordinated epithelial stress response characterized by inflammatory and metabolic pathway enrichment. The results show that\n                    <jats:italic>EGR1<\/jats:italic>\n                    is associated with epithelial autophagy\u2010related alterations under allergic stimulation, and these changes are accompanied by augmented release of the alarmin IL\u201033. These observations support a conceptual framework wherein\n                    <jats:italic>EGR1<\/jats:italic>\n                    \u2010linked autophagy\u2010associated processes may contribute to epithelial stress responses during early inflammatory events in allergic airway disease. Elucidation of the precise molecular underpinnings and causal relationships awaits further investigation.\n                  <\/jats:p>","DOI":"10.1002\/pdi3.70075","type":"journal-article","created":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T06:31:38Z","timestamp":1790404298000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Early Growth Response 1\u2010Associated Epithelial Autophagy\u2010Related Changes in Allergic Airway Inflammation"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-6574-6575","authenticated-orcid":false,"given":"Xinyang","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Respiratory Medicine Children's Hospital of Chongqing Medical University, National Clinical Research Center for Children and Adolescents' Health and Diseases, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing Municipal Health Commission Key Laboratory of Children's Vital Organ Development and Diseases  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of Respiratory Medicine Children's Hospital of Chongqing Medical University, National Clinical Research Center for Children and Adolescents' Health and Diseases, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing Municipal Health Commission Key Laboratory of Children's Vital Organ Development and Diseases  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Respiratory Medicine Children's Hospital of Chongqing Medical University, National Clinical Research Center for Children and Adolescents' Health and Diseases, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing Municipal Health Commission Key Laboratory of Children's Vital Organ Development and Diseases  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhengxiu","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Respiratory Medicine Children's Hospital of Chongqing Medical University, National Clinical Research Center for Children and Adolescents' Health and Diseases, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing Municipal Health Commission Key Laboratory of Children's Vital Organ Development and Diseases  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,25]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140\u20106736(17)33311\u20101"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/nri3786"},{"key":"e_1_2_11_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.3045"},{"key":"e_1_2_11_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2737"},{"key":"e_1_2_11_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2015.07.007"},{"key":"e_1_2_11_7_1","doi-asserted-by":"publisher","DOI":"10.3390\/cells11071105"},{"key":"e_1_2_11_8_1","doi-asserted-by":"publisher","DOI":"10.1111\/imr.12619"},{"key":"e_1_2_11_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/nri.2016.95"},{"key":"e_1_2_11_10_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0906312"},{"key":"e_1_2_11_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.3049"},{"key":"e_1_2_11_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2018.09.048"},{"key":"e_1_2_11_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2011.10.026"},{"key":"e_1_2_11_14_1","doi-asserted-by":"publisher","DOI":"10.1111\/all.12761"},{"key":"e_1_2_11_15_1","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2014.00244"},{"key":"e_1_2_11_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2019.05.026"},{"issue":"4","key":"e_1_2_11_17_1","first-page":"226","article-title":"Early Growth Response 1\u2014A Transcription Factor in the Crossfire of Signal Transduction Cascades","volume":"48","author":"Pagel J. 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