Editorial on the Research Topic: The Different Faces of Sickness
Sickness not only includes symptoms that classically define an infection (e.g., fever, nausea, headache), but also comes along with profound neurobehavioral consequences for the infected individual. These include anhedonia, anorexia, pain, lethargy, fatigue, sleepiness, and social withdrawal, and are collectively called “sickness behavior” (1). Sickness behavior in the infected individual is triggered by mediators of the activated immune system that signal to the brain, thus linking the immunological (inflammatory) response with the psychological (behavioral) response to a pathogen. These inflammatory mediators include cytokines (e.g., interleukins, IL; tumor necrosis factor, TNF) that can be assessed in the circulation in addition to clinical markers of inflammation (e.g., C-reactive protein, CRP). Inflammation and sickness behavior are paralleled by neuroendocrine changes including activation of the autonomic nervous system and the hypothalamus-pituitary-adrenal (HPA) axis (1), which are both critical for the feedback regulation of the immune response.