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The cytokine interleukin\u20101\u03b1 has been demonstrated to act as an alarmin released by necrotic cells. In the present study, we investigated the influence of IL\u20101\u03b1 on the immune response during acute and chronic pancreatitis. Following tissue injury, pancreatic acinar cells released IL\u20101\u03b1, which activates tissue\u2010resident fibroblasts to differentiate toward a pro\u2010inflammatory phenotype. By secreting chemokines and cytokines such as CXCL5, CCL2, and IL\u20106, these fibroblasts recruit immune cells to the pancreas. The absence of IL\u20101\u03b1 reduces disease severity in acute pancreatitis and chemokine release. Furthermore, IL\u20101\u03b1 primes fibroblasts to enhance the production of extracellular matrix\u2010components by the up\u2010regulation of pro\u2010fibrotic receptors such as\n                    <jats:italic>Il4ra<\/jats:italic>\n                    ,\n                    <jats:italic>Il13ra1<\/jats:italic>\n                    , and\n                    <jats:italic>Tgfbr3<\/jats:italic>\n                    . Therefore, the deletion of IL\u20101\u03b1 significantly reduced the development of tissue fibrosis. A therapeutic blockade of the IL1R1\u2010signaling by i.p. administration of the IL\u20101\u2010receptor antagonist Anakinra showed the same effect; the severity of acute pancreatitis and fibrogenesis during chronic pancreatitis were reduced. In conclusion, the crosstalk between necrotic acinar cells and fibroblasts mediated by IL\u20101\u03b1 plays a crucial role in acute inflammation of the pancreas and fibrogenic signaling. Blockade of IL1R1\u2010signaling by Anakinra is therefore a promising therapeutic intervention for both acute and chronic pancreatitis.\n                  <\/jats:p>","DOI":"10.1002\/advs.77558","type":"journal-article","created":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T05:01:56Z","timestamp":1788498116000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Interleukin\u20101\u03b1 Mediates Pancreatic Fibroblast Activation, Regulates Immune Cell Recruitment and Fibrosis in Acute and Chronic Pancreatitis"],"prefix":"10.1002","author":[{"given":"Hala","family":"Mazloum","sequence":"first","affiliation":[{"name":"Department of Medicine A University Medicine Greifswald  Greifswald Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shenja","family":"Buchholz","sequence":"additional","affiliation":[{"name":"Department of Medicine A University Medicine Greifswald  Greifswald 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