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Updated: Mar 8, 2026

Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue
Published on: October 12, 2013
Interleukin-36α Induces Inflammatory Mediators From Human Pancreatic Myofibroblasts Via a MyD88 Dependent Pathway
Atsushi Nishida1, Osamu Inatomi, Takehide Fujimoto
1From the Department of Medicine, Shiga University of Medical Science, Otsu, Japan.
Objectives:
Interleukin-36 (IL-36) is a recently described proinflammatory cytokine, characterized by the induction of inflammatory mediators. In the present study, we investigated the biological activity and the signal transduction of IL-36α in human pancreatic myofibroblasts.
Methods:
The mRNA and protein expression of inflammatory mediators was evaluated using real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The expression of IL-36α and its receptor in the pancreatic tissue was evaluated using immunohistochemical technique. Intracellular signaling pathways were evaluated using immunoblotting and specific small interference RNA-transfected cells.
Results:
Interleukin-36α and its receptor complex IL-36R/IL-1RAcP were detected in fibrotic tissue of chronic pancreatitis. Interleukin-36α dose- and time-dependently induced the mRNA expression and protein secretion of CXCL1, CXCL8, MMP-1, and MMP-3 from human pancreatic myofibroblasts. Interleukin-36α assembled MyD88 adaptor proteins (MyD88, TRAF6, IRAK1, and TAK1) into a complex. Furthermore, IL-36α induced the phosphorylation of mitogen-activated protein kinases and the activation of nuclear factor κB and activator protein 1. Mitogen-activated protein kinase inhibitors and small interference RNAs specific for nuclear factor κB and activator protein 1 significantly suppressed the protein secretion of inflammatory mediators induced by IL-36α stimulation.
Conclusions:
It was suggested that IL-36α plays an important role in the pathophysiology of inflammation and fibrosis in the pancreas via an autocrine function.
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