{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T17:56:33Z","timestamp":1772387793416,"version":"3.50.1"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T00:00:00Z","timestamp":1769904000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"University of South Alabama College of Medicine","award":["MOWYCAL LLC"],"award-info":[{"award-number":["MOWYCAL LLC"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,2,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Autosomal dominant hyper-IgE syndrome (AD-HIES), or Job\u2019s syndrome, is a rare primary immunodeficiency caused by dominant-negative mutations in STAT3. Patients experience recurrent pulmonary infections and chronic inflammation, leading to severe complications and heightened mortality risk. To investigate whether neutrophil-intrinsic dysfunction contributes to lung pathology in AD-HIES, we used a murine model expressing the STAT3V463\u0394 mutation, a common disease-associated variant. Following intratracheal infection with Pseudomonas aeruginosa, STAT3V463\u0394 mice exhibited pronounced alveolar damage, increased vascular congestion, and extensive leukocyte infiltration compared to wild-type (WT) controls. These changes were accompanied by elevated bacterial burden and significantly increased levels of pro-inflammatory cytokines and chemokines in the lung. Neutrophil recruitment to the lungs was markedly elevated, and surface expression of degranulation markers was enhanced in STAT3V463\u0394 neutrophils in vivo. To determine whether neutrophil hyperactivation was driven by intrinsic defects independent of microbial load, mice were challenged intratracheally with purified lipopolysaccharide (LPS), revealing similarly enhanced neutrophil degranulation and NETosis in STAT3V463\u0394 mice despite controlled PAMP exposure. Mechanistically, bone marrow\u2013derived neutrophils (BMDNs) from STAT3V463\u0394 mice displayed heightened degranulation and NETosis in response to PMA or f-MLF stimulation. Together, these findings demonstrate that STAT3V463\u0394 drives neutrophil hyperresponsiveness, contributing to dysregulated inflammation and pulmonary tissue damage in AD-HIES.<\/jats:p>","DOI":"10.1093\/jimmun\/vkaf373","type":"journal-article","created":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T17:13:34Z","timestamp":1772385214000},"source":"Crossref","is-referenced-by-count":0,"title":["Neutrophil hyperresponsiveness contributes to lung pathology in\n                    <i>STAT3V463\u0394<\/i>\n                    mice"],"prefix":"10.1093","volume":"215","author":[{"given":"Killian Zane","family":"Brewer","sequence":"first","affiliation":[{"name":"Department of Microbiology & Immunology, University of South Alabama, Mobile , AL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Madeline","family":"Stone","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of South Alabama, Mobile , AL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rachael L","family":"Motamed","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, University of South Alabama, Mobile , AL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ryan","family":"Walde","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of South Alabama, Mobile , AL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Domenico","family":"Spadafora","sequence":"additional","affiliation":[{"name":"Flow Cytometry Shared Resource Laboratory, University of South Alabama, Mobile, AL, United States"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jonathan P","family":"Audia","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, University of South Alabama, Mobile , AL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sarah","family":"Sayner","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of South Alabama, Mobile , AL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5713-5369","authenticated-orcid":false,"given":"Robert A","family":"Barrington","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, University of South Alabama, Mobile , AL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2026,3,1]]},"reference":[{"key":"2026030112132127800_vkaf373-B1","doi-asserted-by":"crossref","first-page":"1058","DOI":"10.1038\/nature06096","article-title":"Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome","volume":"448","author":"Minegishi","year":"2007","journal-title":"Nature"},{"key":"2026030112132127800_vkaf373-B2","doi-asserted-by":"crossref","first-page":"1608","DOI":"10.1056\/NEJMoa073687","article-title":"STAT3 mutations in the hyper-IgE syndrome","volume":"357","author":"Holland","year":"2007","journal-title":"N Engl J Med"},{"key":"2026030112132127800_vkaf373-B3","doi-asserted-by":"crossref","first-page":"424","DOI":"10.1016\/j.jaci.2009.10.059","article-title":"Mutations in STAT3 and diagnostic guidelines for hyper-IgE syndrome","volume":"125","author":"Woellner","year":"2010","journal-title":"J Allergy Clin Immunol"},{"key":"2026030112132127800_vkaf373-B4","doi-asserted-by":"crossref","first-page":"2978","DOI":"10.1182\/blood-2013-09-523167","article-title":"A mouse model of HIES reveals pro- and anti-inflammatory functions of STAT3","volume":"123","author":"Steward-Tharp","year":"2014","journal-title":"Blood"},{"key":"2026030112132127800_vkaf373-B5","doi-asserted-by":"crossref","first-page":"5582","DOI":"10.1097\/MS9.0000000000002407","article-title":"Challenges in diagnosing and managing hyper-IgE syndrome in a resource-limited setting: a case report","volume":"86","author":"Adhikari","year":"2024","journal-title":"Ann Med Surg (Lond)"},{"key":"2026030112132127800_vkaf373-B6","doi-asserted-by":"crossref","first-page":"49","DOI":"10.1006\/clim.2001.5039","article-title":"Cytokine and chemokine dysregulation in hyper-IgE syndrome","volume":"100","author":"Chehimi","year":"2001","journal-title":"Clin Immunol"},{"key":"2026030112132127800_vkaf373-B7","doi-asserted-by":"crossref","first-page":"100270","DOI":"10.1016\/j.opresp.2023.100270","article-title":"Hyper IgE syndrome with multiple respiratory infections. 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