{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:07:08Z","timestamp":1791295628990,"version":"4.1.0"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2024,8,10]],"date-time":"2024-08-10T00:00:00Z","timestamp":1723248000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100018353","name":"European Crohn\u2019s and Colitis Organization","doi-asserted-by":"crossref","award":["2020"],"award-info":[{"award-number":["2020"]}],"id":[{"id":"10.13039\/100018353","id-type":"DOI","asserted-by":"crossref"}]},{"name":"University Hospitals Leuven"},{"name":"KU Leuven Global PhD Partnerships with the University of Edinburgh","award":["GPUE\/20"],"award-info":[{"award-number":["GPUE\/20"]}]},{"name":"KU Leuven Internal Funds","award":["C12\/15\/016"],"award-info":[{"award-number":["C12\/15\/016"]}]},{"name":"KU Leuven Internal Funds","award":["C14\/17\/097"],"award-info":[{"award-number":["C14\/17\/097"]}]},{"DOI":"10.13039\/501100003130","name":"Fonds Wetenschappelijk Onderzoek","doi-asserted-by":"publisher","award":["G086721N"],"award-info":[{"award-number":["G086721N"]}],"id":[{"id":"10.13039\/501100003130","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003130","name":"Fonds Wetenschappelijk Onderzoek","doi-asserted-by":"publisher","award":["S008419N"],"award-info":[{"award-number":["S008419N"]}],"id":[{"id":"10.13039\/501100003130","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003130","name":"Fonds Wetenschappelijk Onderzoek","doi-asserted-by":"publisher","award":["1514518N"],"award-info":[{"award-number":["1514518N"]}],"id":[{"id":"10.13039\/501100003130","id-type":"DOI","asserted-by":"publisher"}]},{"name":"European Union\u2019s Horizon Europe Research & Innovation program","award":["FIBROTARGET"],"award-info":[{"award-number":["FIBROTARGET"]}]},{"name":"European Union\u2019s Horizon Europe Research & Innovation program","award":["101080523"],"award-info":[{"award-number":["101080523"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,1,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background and Aims<\/jats:title>\n                  <jats:p>During early phases of inflammation, activated neutrophils extrude neutrophil extracellular traps (NETs) in a peptidyl arginine deiminase 4 (PAD4)-dependent manner, aggravating tissue injury and remodeling. In this study, we investigated the potential pro-fibrotic properties and signaling of NETs in Crohn\u2019s disease (CD).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>NETs and activated fibroblasts were labeled on resected ileum from CD patients by multiplex immunofluorescence staining. NETs-treated human primary intestinal fibroblasts were analyzed by bulk RNA sequencing to uncover cell signaling pathways, and by high-throughput imaging to assess collagen production and migratory activity. Consequentially, TLR2\/NF-\u03baB pathway was evaluated by transfection of CCD-18Co fibroblasts with an NF-\u03baB-luciferase reporter plasmid, incorporating C29 to block TLR2 signaling. A chronic dextran sulfate sodium (DSS) mouse model was used to define the specific role of PAD4 deletion in neutrophils (MRP8-Cre, Pad4fl\/fl).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Immunofluorescence showed spatial colocalization of NETs and activated fibroblasts in ileal ulcerations of CD patients. Transcriptomic analysis revealed upregulation of pro-fibrotic genes and activation of Toll-like receptor signaling pathways in NETs-treated fibroblasts. NETs treatment induced fibroblast proliferation, diminished migratory capability, and increased collagen release. Transfection experiments indicated a substantial increase in an NF-\u03baB expression with NETs, whereas C29 led to decreased expression and release of collagen. In line, a significant reduction in collagen content was observed in the colon of MRP8-Cre, Pad4fl\/fl mice subjected to chronic DSS colitis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>NETs potentially serve as an initial stimulus for pathological activation of fibroblasts within the intestine via the TLR2\/NF-\u03baB pathway. Given their early involvement in inflammation, inhibition of PAD4 might offer a strategy to modulate both inflammation and fibrogenesis in CD.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ecco-jcc\/jjae121","type":"journal-article","created":{"date-parts":[[2024,8,10]],"date-time":"2024-08-10T10:48:35Z","timestamp":1723286915000},"source":"Crossref","is-referenced-by-count":16,"title":["The Impact of Peptidyl Arginine Deiminase 4-Dependent Neutrophil Extracellular Trap Formation on the Early Development of Intestinal Fibrosis in Crohn\u2019s Disease"],"prefix":"10.1093","volume":"19","author":[{"given":"Gabriele","family":"Dragoni","sequence":"first","affiliation":[{"name":"Translational Research Center for Gastrointestinal Disorders (TARGID), KU\u00a0Leuven Department of Chronic Diseases and Metabolism, , Leuven ,\u00a0","place":["Belgium"]},{"name":"Gastroenterology Research Unit, Department of Experimental and Clinical Biochemical Sciences \u201cMario Serio\u201d, 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