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Expression of interleukin-24 and its receptor in human pancreatic myofibroblasts
Hirotsugu Imaeda1, Atsushi Nishida, Osamu Inatomi
1Department of Medicine, Graduate School of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu, Japan.
Insights
Interleukin-24 (IL-24) is present in chronic pancreatitis tissues, specifically in myofibroblasts. Its expression is induced by IL-1β through the AP-1 pathway, suggesting a role in pancreatitis.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Interleukin-24 (IL-24) belongs to the IL-10 family of cytokines.
- Chronic pancreatitis is characterized by inflammation and fibrosis of the pancreas.
Purpose of the Study:
- To investigate IL-24 expression in chronic pancreatitis tissues.
- To elucidate the molecular mechanisms regulating IL-24 expression in human pancreatic myofibroblasts.
Main Methods:
- Immunohistochemistry was used to evaluate IL-24 expression in tissues.
- Real-time PCR and ELISA assessed IL-24 mRNA and protein levels in myofibroblasts.
- Inhibitors of p38 MAPK, PI3K, and AP-1 (c-Jun) were employed to study signaling pathways.
Main Results:
- IL-24 was detected in α-smooth muscle actin-positive myofibroblasts within chronic pancreatitis tissues.
- IL-1β significantly upregulated IL-24 mRNA and protein expression in pancreatic myofibroblasts.
- IL-1β-induced IL-24 expression was mediated by the transcription factor AP-1, involving p38 MAPK and PI3K signaling.
- Pancreatic myofibroblasts express IL-22R1, IL-20R1, and IL-20R2, and IL-24 induced phosphorylation of p42/44, p38, JNK, and STAT1/3.
Conclusions:
- IL-24 is expressed in chronic pancreatitis tissue by myofibroblasts.
- IL-24 may contribute to the pathophysiology of chronic pancreatitis through autocrine signaling pathways.
Abstract:
Interleukin (IL)-24 is a member of the IL-10 family of cytokines. In this study, we investigated IL-24 expression in chronic pancreatitis tissue and characterized the molecular mechanisms responsible for IL-24 expression in human pancreatic myofibroblasts. IL-24 expression in the tissues was evaluated by immunohistochemical methods. IL-24 mRNA and protein expression in the pancreatic myofibroblasts was determined by real-time-PCR and ELISA, respectively. IL-24 was expressed by α-smooth muscle actin-positive myofibroblasts in the chronic pancreatitis tissues. In isolated human pancreatic myofibroblasts, IL-1β significantly enhanced IL-24 mRNA and protein expression. The p38 MAPK inhibitor SB203580 and the PI3K inhibitor LY294002 significantly reduced the IL-β-induced IL-24 mRNA expression. An adenovirus containing a dominant-negative mutant of c-Jun significantly inhibited the effects of IL-1β on IL-24 mRNA expression, indicating that the IL-1β-induced IL-24 mRNA expression was mediated by the activation of transcription factor AP-1. Pancreatic myofibroblasts expressed IL-22R1, IL-20R1 and IL-20R2, and recombinant IL-24 induced the phosphorylation of p42/44, p38, JNK and STAT1/3. IL-24 is expressed in chronic pancreatitis tissue, and may play a role in the pathophysiology of chronic pancreatitis via autocrine pathways.
