In addition, studies of the immune function of children suffering from irritable bowel syndrome have shown that a low dose of γ internal irradiation significantly changes their

innate immune function and also leads to significant decreases in the macrophage activity and phagocytic index ( Sheikh Sajjadieh et al., 2010). However, Gazin et al. (2004) found that exposure of the NR8383 macrophages to uranium (50 μM) for 24 hours causes increased secretion of TNF-α, whereas the secretion of IL-1β and IL-10 is not affected by uranium exposure. We believe that these inconsistent results stem from the fact that the present study employed in vivo experiments to investigate the effect of long-term exposure to relatively low doses of DU. Second, long-term exposure to DU

caused changes in the humoral immune STA-9090 solubility dmso function of the mice. In particular, when the dose of uranium in the feed exceeded 30 mg/kg, the total serum IgG and IgE levels increased, the proliferative capacity of splenic B cells was enhanced, and the proportion of mIgM+mIgD+ double-positive B cells increased; the serum IgG level did not change significantly in the DU3 group (3 mg/kg), but the serum IgE level was significantly increased. IgG is the product of the secondary immune response, and IgE mainly mediates allergic Epacadostat mw reactions. The increase in the IgG and IgE levels strongly suggested that chronic exposure to DU might increase the susceptibility to allergic disease. At present, the researchers of lead exposure-induced immunotoxicity have not reached a consensus regarding the change in the total serum IgM and IgG levels. Generally, a sufficiently high dose and long exposure time leads to a decrease in the total serum IgM and IgG levels, while a short-term

exposure at a low dose increases the total serum IgM and IgG levels. However, an increased serum IgE level has been recognised as the one of the significant markers 4��8C of lead-induced immunotoxicity (Dietert and Piepenbrink, 2006). This study also found that the chronic exposure to DU led to greater proliferative ability of splenic B cells stimulated by LPS, further suggesting that the DU exposure may promote the B cell-mediated humoral immune function. This result is different from those from acute exposure to large doses of DU. The results of our previous study (Hao et al., 2012a) showed that in four days after intraperitoneal injection of DU (10 mg/kg body weight), the proliferative ability of the splenic B cells was decreased.