Somatostatin Inhibits the Production of Interferon-γ by Intestinal Epithelial Cells During Intestinal Ischemia–Reperfusion in Macaques

BACKGROUND: Our previous study found that somatostatin (SST) inhibited the intestinal inflammatory injury in a macaque model of intestinal ischemia–reperfusion (IIR); however, the underlying mechanism was unclear. AIMS: The present study was aimed to investigate the effects of SST on IFN-γ and the systemic inflammatory response after IIR. METHODS: Fifteen macaques were randomly divided into controls, IIR and SST+ IIR groups. ELISA was performed to measure IFN-γ in ileum tissues, ileac epithelial cells (IECs) and ileal lymphocytes, as well as the systemic levels of IL-6, IL-1β, TNF-α and IFN-γ in the peripheral circulation and the portal vein. HE staining was performed to evaluate morphological changes in vital organs. Immunohistochemistry was performed to identify the distribution of IFN-γ, CD4, CD8 and CD57 in the ileum. RESULTS: After IIR, IFN-γ level was significantly increased in the IECs. IL-6, IL-1β and TNF-α were significantly increased in both the portal vein and the peripheral circulation; in contrast, IFN-γ level was increased in the portal vein alone. Prophylactic SST reversed the change in IFN-γ in the IECs and portal vein. SST led to an alleviation of the pathological changes in systemic vital organs. The distribution of CD4(+), CD57(+) and CD8(+) cells was not positively correlated with the secretion of IFN-γ. CONCLUSION: IECs are the main source of IFN-γ production after IIR. SST may indirectly lead to mast cell deactivation through the inhibition of IFN-γ production by IECs. Pretreatment with SST may be beneficial for preventing a massive systemic inflammatory response in vital organs after IIR.