The inflammatory response of the innate immune system is thought to contribute to the pathophysiology of some types of depression. Depression is associated with elevated levels of markers of systemic inflammation (eg, C-reactive protein) as well as inflammatory cytokines such as interleukin-6 and tumor necrosis factor-α. In addition, both C-reactive protein and inflammatory cytokines are reported to correlate prospectively with the onset of major depressive disorder (Slavich and Irwin, 2014). Increasingly, experimental paradigms have been used to evaluate the causal role of inflammation on depressive symptoms, given evidence that acute inflammatory reactivity to laboratory-based challenges is clinically meaningful in predicting increases in depression over the following year (Slavich and Irwin, 2014). Indeed, one model of experimentally induced inflammation, endotoxin administration, can serve as a potent approach to interrogate the role of inflammation on depressive symptom induction, and to identify the neurobiological substrates that subserve these clinical changes (Schedlowski et al, 2014).

Endotoxin administration induces two cardinal affective symptoms, depressed mood and anhedonia, which are key elements of depression (Schedlowski et al, 2014). Whereas the current diagnostic criterion of anhedonia can be met through demonstrated ‘loss of interest or pleasure’, the ‘wanting’ and ‘liking’ aspects of anhedonia may represent different components of reward behavior. In this study, Lasselin et al (2016) addressed this question, examined how inflammation influences anhedonia, and tested whether inflammation and associated subjective states such as sleepiness alter motivation, sensitivity to monetary reward, or both (Lasselin et al, 2016). In so doing, the findings of Lasselin et al (2016) challenge a widely accepted view that inflammation reduces incentive motivation or the willingness to expend effort to obtain a reward (Lasselin et al, 2016) and further suggest that diagnostic ‘lumping’ of interest and pleasure may be out of step with neurobiological reality (Felger and Treadway, 2016).

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