The efficacy of intravenous immunoglobulin on lipopolysaccharide-induced fetal brain inflammation in preterm rats.

Abstract

Interleukin-1 is accepted as one of the major cytokines; it is involved in inflammatory processes and systemic fetal inflammatory response that is triggered by maternal lipopolysaccharide (LPS) injection. Because it is an antiinflammatory agent, we investigated (in the brain damage of rat pups) the role of intravenous immunoglobulin (IVIG) in decreasing interleukin-1 beta (IL-1β) expression and caspase 3 activity that was induced by maternal LPS administration. Dams were divided into 3 groups. Pyrogen-free saline solution (NS) was administered intraperitoneally to group 1; LPS (0.3 mg/kg) suspension in NS was administered to groups 2 and 3 at 19 days of gestation. Two hours after the first injection, a second injection of NS was administered intravenously to group 1 (NS + NS), of IVIG was administered intravenously to group 2 (LPS + IVIG), and of NS was administered intravenously to group 3 (LPS + NS). Hysterectomy was performed in one-half of the dams 2 hours after the second injection and in the other one-half of the dams 22 hours after the second injection. Pups were delivered, and the brains were extracted just after delivery. IL-1β expression and caspase 3 activity were determined in brain tissues. For the pups at 4 hours, the IL-1β expression of group 2 was significantly lower than groups 1 and 3. For the pups at 24 hours, the IL-1β expression of group 2 was significantly lower than group 3 but was similar to group 1. For the pups at 24 hours, caspase 3 activity of groups 1 and 2 were significantly lower than group 3. Maternal IVIG administration decreased IL-1β expression and caspase 3 activity in the brain tissue of rat pups, which had been induced by maternal LPS-administration.