Where does inflammation in insomnia come from? and does it matter for comorbidity?

This is the authors' abstract. We don't add key points for this paper.

Among the various adaptive functions of normal sleep, the regulation of immune system historically received much attention in basic sleep science [1–5]. Inflammation can be defined as an evolutionary-based primary defense of the body against physical or psychosocial threats. Inflammation is therefore a normal and adaptive process as far as it is proportionate and directed to the appropriate target. Substantial abnormalities in the timing and strength of inflammatory response can instead cause acute or chronic illness [6]. Thus, a traditional contribution of sleep research to this field regarded how sleep could influence the trajectories from normal to pathological inflammatory response [5, 7]. Major findings in this context highlighted, for example, that sleep deprivation may induce chronobiological changes in proinflammatory markers secretion [8] and promote the activation of nuclear factor-kappaB, which is a key transcriptional control pathway in the inflammatory response [4]. More recently, several research groups attempted to translate basic knowledge about the sleep-immune pathways into the study of clinically relevant topics. These included the role of experimentally induced sleep loss and sleep disorders (i.e. insomnia) in the pathophysiology of inflammation-related diseases (e.g. [9–14], and mortality [15–17]), the interactions between inflammatory markers and pathological sleep conditions in influencing mental health [18–21], as well as the efficacy of sleep-promoting interventions, i.e. cognitive behavioral therapy for insomnia (CBT-I), in reducing inflammation [22–24].