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Updated: May 5, 2026
Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice
Published on: March 10, 2017
Insulinlike growth factor I and interleukin 1 beta messenger RNA in a rat model of granulomatous enterocolitis and
E M Zimmermann1, R B Sartor, R D McCall
1Department of Internal Medicine, University of Michigan, Ann Arbor.
Background:
Insulinlike growth factor I (IGF-I) is mitogenic for fibroblasts and smooth muscle cells and stimulates collagen synthesis. The present study tested the hypothesis that IGF-I is important in the development of granulomatous inflammation and fibrosis.
Methods:
IGF-I messenger RNA (mRNA) was measured in bowel and liver of rats with peptidoglycan-polysaccharide-induced chronic granulomatous enterocolitis and hepatitis using RNase protection. Cellular sites of IGF-I mRNA and IGF-I peptide precursor were localized by in situ hybridization and immunohistochemistry, respectively. Sites of IGF-I synthesis were compared with sites of interleukin 1 beta mRNA expression.
Results:
IGF-I mRNA was increased 3.7-fold in cecal tissue from peptidoglycan-polysaccharide-injected rats compared with controls. IGF-I mRNA was up-regulated in fibroblastlike cells in the intensely fibrotic periphery of cecal and hepatic granulomas. This region also expressed IGF-I peptide precursor. Interleukin 1 mRNA localized to macrophage-like cells in the center of granulomas.
Conclusions:
IGF-I may be important in the development of fibrosis in this model of Crohn's disease. The localization of IGF-I and interleukin 1 mRNAs to distinct but adjacent sites is consistent with a paracrine interaction between cells expressing IGF-I and interleukin 1.
