Temporal effects of intestinal ischemia/reperfusion in phagocytosis and inflammatory mediators release

Abstract

Intestinal ischemia/reperfusion (i-I/R) can induce acute lung inflammation. Furthermore, injuries seen in i-I/R may cause deterioration of the immune system. Studies have demonstrated that dendritic cells present lower responsiveness to bacterial components, while peritoneal macrophages reduce the levels of MHC-II and release less IL-12. Male Wistar rats were subjected to 45 min of ischemia of the superior mesenteric artery and then to 2 h, 3, 5 or 20 days of reperfusion. After these times, the phagocytosis and oxidative burst of peritoneal macrophages and blood monocytes were evaluated by flow cytometry. In addition, inflammatory mediators were quantified in lung culture. We observed that after 5 days of reperfusion the phagocytosis of monocytes was lower than in basal and in the other periods studied. On the other hand, the oxidative burst in this time increased. The phagocytosis of peritoneal macrophages increased after 3 and 5 days of reperfusion, while the oxidative burst increased only after 3 days. Lung explants culture from reperfused rats revealed that while the levels of IL-1β increased during the days of reperfusion, the levels of IL-10 decreased. Furthermore, the amount of IL-17A, TNF-α and IL-4 were higher after 5 days of reperfusion than in the others times. Our data indicate the i-I/R as a promoter of temporal changes in the immune system that alter its ability to maintain the homeostasis and to respond appropriately to pathogens.