Oxidative damage and
inflammation occur early in the brain after
sepsis and are resolved when long-term
cognitive impairment occurs. There is no information of a direct relation between acute levels of
brain inflammation and oxidative damage and long-term cognitive deficits. We hypothesized that higher levels of early oxidative damage and
inflammation are followed by long-term cognitive deficits, and this is related to a decrease in the levels of brain-derived neurotropic factor (
BDNF). Wistar rats were subjected to
sham operation or cecal
ligation and perforation and the cerebrospinal fluid (CSF) was obtained 6 and 24 h after the determination of
thiobarbituric acid-reactive species,
interleukin 1 (IL-1),
IL-10, and
tumor necrosis factor α (TNF-α). Animals were followed until 30 days after surgery and were subjected to the step-down inhibitory avoidance (IA) task, and the hippocampus levels of
BDNF were determined. At 6 h, higher CSF levels of
thiobarbituric acid-reactive species and TNF-α were observed in septic animals that had a better performance in the IA task and presented higher
BDNF levels in the hippocampus. At 24 h, higher CSF levels of IL-1β and TNF-α were observed in septic animals that had a worse performance in the IA task, and this was associated with lower
BDNF levels. The persistence of
brain inflammation during the acute phase of
sepsis is associated with long-term hippocampus levels of
BDNF and memory impairment in
sepsis survivors.