Abstract
The 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.
Highlights
The pathogenesis of some chronic inflammation such as inflammatory bowel disease is unclear
The results showed that intestinal epithelial cells expressed Insulin-like growth factor-1 (IGF1); the latter promoted the expression of IL-10 in Mos
Published data indicate that both IGF122 and CpG-ODN23 are involved in regulating in the intestinal epithelial cell (IEC) activities
Summary
The 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. The IGF1-primed Mos showed the immune suppressive effect on inhibiting the immune inflammation in the mouse colon. The IGF1-primed Mos are capable of suppressing immune inflammation in the intestine. Mos differentiate into dendritic cells or macrophages, which are directly involved in multiple immune responses[6]. The external stimulation may activate IECs and induce IECs to produce molecules to influence the immune cell functions in the sub-epithelial region[10]. Whether IECs produce some other growth factors, such as insulin-like growth factor-1 (IGF1), has not been fully understood. Whether IGF can regulate the inflammatory process in the intestine has not been investigated
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