Insulin-like growth factor-1 endues monocytes with immune suppressive ability to inhibit inflammation in the intestine

• DOI: 10.1038/srep07735
• Publication Date: 2015-01-15T10:28:42Z
• Authors: Rong-Ti Ge; Li-Hua Mo; Ruijin Wu; Jiang-Qi Liu; Huan-Ping Zhang; Zhigang Liu; Zhanju Liu; Ping-Chang Yang
• Keywords: Immunosuppression Therapy; Inflammation; 0301 basic medicine; Mice, Inbred BALB C; 0303 health sciences; Lipopolysaccharide Receptors; Epithelial Cells; Cell Separation; Colitis; 16. Peace & justice; Article; Monocytes; Cell Line; Interleukin-10; Receptor, IGF Type 1; Intestines; 03 medical and health sciences; Phenotype; Oligodeoxyribonucleotides; Trinitrobenzenesulfonic Acid; Animals; Insulin-Like Growth Factor I; Spleen

AbstractThe pathogenesis of some chronic inflammation such as inflammatory bowel disease is unclear. Insulin-like growth factor-1 (IGF1) has active immune regulatory capability. This study aims to investigate into the mechanism by which IGF1 modulates the monocyte (Mo) properties to inhibit immune inflammation in the intestine. In this study, the production of IGF1 by intestinal epithelial cells was evaluated by real time RT-PCR and Western blotting. Mos were analyzed by flow cytometry. A mouse colitis model was created with trinitrobenzene sulfonic acid. The results showed that mouse IECs produced IGF1, which could be up regulated by exposure to CpG-ODN (CpG-oligodeoxynueleotides) in the culture. Culture the CpG-ODN-primed IEC cells and Mos or exposure of Mos to IGF1 in the culture induced the Mos to express IL-10. The IGF1-primed Mos showed the immune suppressive effect on inhibiting the immune inflammation in the mouse colon. In conclusion, the IGF1-primed Mos are capable of suppressing immune inflammation in the intestine.