ArticleScientific reports2026
IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Chronic Pancreatitis (CP) is a progressive inflammatory disease leading to fibrosis. The role of interleukin-18 (IL-18), an inflammation-associated cytokine, in CP, especially its interactions with pancreatic stellate cells (PSCs) and macrophages, remains unclear. Human CP tissues and caerulein-induced CP models in mice were used to explore the role of IL-18 in fibrosis. Histopathological analysis, immunofluorescence, and in vitro co-culture systems were employed to identify cellular targets and downstream signaling of IL-18. IL-18 expression was elevated in CP pancreata, correlating with the severity of fibrosis. Deletion of IL-18Rα reduced fibrosis, PSC activation, and macrophage M2 polarization in CP mice. IL-18 directly stimulated PSCs to secrete interleukin-4 (IL-4), which induced M2 polarization of macrophages, exacerbating fibrosis. Inhibition of IL-4 alleviated fibrosis and M2 polarization. IL-18 plays a critical role in driving pancreatic fibrosis by modulating PSCs-macrophage interactions, providing a potential therapeutic target to disrupt the fibrotic process in CP.
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