Neonatal endotoxin exposure impairs avoidance learning and attenuates endotoxin-induced sickness behavior and central IL-1beta gene transcription in adulthood.

Infection during infancy, a time of critical neural development, may have long-term implications. Infection or exposure to an immune stimulus such as lipopolysaccharide (LPS) early in life leads to alterations in the reactivity of the hypothalamic-pituitary-adrenal axis (HPA) and febrile response in adulthood. Relatively few studies have assessed the behavioral and cognitive alterations induced by perinatal immune challenge.