To prove this, the team studied several leptin-deficient mouse models, including one that was missing leptin receptors everywhere except within the CNS. They report that leptin, long thought to act directly on immune cells themselves, also mediates actions in the CNS. They showed that leptin replacement improved the host response to a standard model of sepsis.

Leptin-dependent neurocircuitry, the authors say, is required for a proper immune response to sepsis, and damage to this circuitry, or even leptin deficiency, may lead to higher risk of death from sepsis.

"Human congenital leptin deficiency is rare," the authors say, "with less than a few dozen patients reported worldwide to date. But there is a stunning number of recorded cases of death due to sepsis in this patient population."

In addition, Tsch-p says, this new finding gives researchers clues that could help in developing therapeutic targets for treating infection in people with damaged leptin-dependent neurocircuitry.

Source: University of Cincinnati Academic Health Center