Abstract
Sepsis complications represent a systemic inflammatory response to microbial infection or severe injury. This study aimed at determining the effects of septic complications in pregnant female mice on the development of their pups. To achieve this aim, pregnant Swiss mice were given an intraperitoneal injection of endotoxin (lipopolysaccharide, LPS) at a single dose of 2.5 mg/kg body weight. Results revealed that bacterial endotoxin increased oxidative stress in both brain and liver tissue. Malondialdehyde (MDA) was significantly elevated in both LPS-treated mothers and their pups. The anti-oxidant enzyme glutathione was significantly reduced in the LPS-treated mothers and their pups. Free radicals induced by endotoxemic stress mediated the pathological and behavioral complications in the pups born to LPS-treated mothers. Thus, obvious damage was observed in hepatic and intestinal tissues, which in turn led to decreased body weight gain and decrease general activity. Spleen sections from treated mothers and pups showed an increase in trabeculae, high leukocyte infiltration (especially neutrophils and immature megakaryocytes). In contrast, significant depletion of neutrophils was detected in peripheral blood. In addition, pups born to LPS-treated mothers showed significantly lower muscular grip strength than that recorded for pups born to control mothers. The active avoidance test indicated that LPS exposure was associated with learning and memory impairment in the pups. In conclusion, septic complications were actively transferred from endotoxin-treated mothers to developing pups, mediated by high oxidative stress. The oxidative stress, hepatic, ileal, splenic and developmental changes were the major determinants in both mothers and pups.