Interleukin-17A as a Potential Mediator in Inflammatory Mechanisms of Insomnia

Abstract

The interaction between immune cytokines and sleep can be bidirectional, and the circadian rhythm balance has a crucial role to the immune and inflammatory regulation. Insomnia is a prevalent sleep disorder, in which occur modifications in immune expression, including the cytokines pattern. Some somnogenic cytokines, such as interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) have been classically recognized for their direct association with sleep behavior and circadian alignment. More recent evidence has increasingly implicated the role of IL-17A in sleep disturbances and neuroinflammation. However, its specific relationship with insomnia disorder remains underexplored. This cytokine is considered as a relevant immune component in the pathways involved in inflammatory and autoimmune issues. Previous and rare studies on the behavior of IL-17A in insomnia related with comorbid disease suggested that increased IL-17A serum levels may be linked to poor sleep quality. We suggest that further experimental and clinical studies examining the role of IL-17A should shed more light in its relationship with insomnia; and on the immunological and neuroinflammatory associations with this sleep disorder.