Sickness is typically associated with suppression of appetite, a phenomenon that can be debilitating, influencing the ability of an individual to withstand pharmacological treatment and ultimately affecting the clinical outcome. This is at least in part due to the ability of the immune system to influence the regulation of energy homeostasis. We found that interleukin 18 (IL-18), a modulator of immune function produced during certain infections or stress, can act centrally to suppress appetite and energy efficiency. By investigating the neurobiology of IL-18 and of its receptors we hope to identify specific pathways that regulate energy homeostasis during sickness which hopefully can become pharmacological targets.
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