Prenatal LPS exposure increases hippocampus IL-10 and prevents short-term memory loss in the male adolescent offspring of high-fat diet fed dams.

Lipopolysaccharide (LPS) tolerance can reduce the neuroinflammation caused by high fat maternal diets; however, there are no reports that have evaluated the effects of prenatal LPS exposure on the memories of the offspring of high-fat diet fed dams. This study evaluated the effects of prenatal LPS exposure on the inflammatory parameters and redox status in the brain, as well as the object recognition memory of adolescent offspring of Wistar rat dams that were treated with a high-fat diet during gestation and lactation. Female pregnant Wistar rats randomly received a standard diet (17.5% fat) or a high-fat diet (45.0% fat) during gestation and lactation. On gestation days 8, 10, and 12, half of the females in each group were intraperitoneally treated with LPS (0.1 mg.kg). After weaning, the male offspring were placed in cages in standard conditions, and at 6 weeks old, animals underwent the novel object recognition test (for short- and long-term memory). The offspring of the high-fat diet fed dams showed increased hippocampus IL-6 levels (21-days-old) and impaired short-term memories. These effects were avoided in the offspring of high-fat diet fed dams submitted to prenatal LPS exposure, which showed greater hippocampus IL-10 levels (at 21- and 50-days-old), increased antioxidant activity (50-days-old) in the hippocampus and prefrontal cortex, without memory impairments (short- and long-term memory). IL-6 has been consistently implicated in memory deficits and as an endogenous mechanism for limiting plasticity, while IL-10 regulates glial activation and has a strong association with improvements in cognitive function. Prenatal LPS exposure preventing the increase of IL-6 in the hippocampus and the impairment to short-term object recognition memory caused by the high-fat maternal diet.