All groups of rats froze the same amount, indicating they had learned. However, immediately after they explored the experimental chamber on the first day, a second group of these rats was injected with a low dose of lipopolysaccharide (LPS), a bacterial component that causes flu-like symptoms,. This time, the rats infected with E. coli as newborns froze 70 percent less often than the rats who'd been injected with salt water as newborns. In other words, under immune stress, the early-infected rats learned to fear the place where they'd been shocked significantly less often than rats who had not been infected as pups. They simply didn't remember it was dangerous.
In a second experiment, the researchers injected 32 different neonatally infected and control adult rats with salt water or with bacterial LPS. Two hours later, they euthenized the rats and checked brain markers of the immune response. Because it spurs an immune response without live bacteria, LPS helps to reveal how the immune system works on its own, without the complication of side effects.
The team found that E. coli-infected pups later injected with LPS had significantly lower concentrations of cytokines called interleukins than control pups (they tested 32 PUPS in all). Immune cells release these cytokines, or certain protein molecules, in response to germs. Prior research had suggested that higher IL-1BETA in the brain's hippocampus, a key memory area, disrupts the consolidation of memories following a learning experience. Thus it appears that there may be an optimal range for IL-1BETA, with either too much or too little inhibiting memory storage. Bilbo says, "The take-home message is that immune responses in a healthy brain are tightly regulated and controlled; any alteration in these responses is likely to cause problems."
'"/>