Innate immune mechanisms of infection: what we know and potential conserved mechanisms affecting sleep during infection

Abstract

Evidence indicates relationships between sleep and the innate immune system during homeostatic sleep and sleep responses after infection. The innate immune system and sleep-like states are highly conserved between simple species and more complex species such as humans. A wide variety of bacteria, viruses, and parasites change sleep patterns in the host during infection. The effects of infection on sleep can occur, in part, due to the bolus and route of infection, prior exposure, immune status of the individual/organism, and the type of pathogen. In addition, elements of circadian patterns and sleep prior to and after infection can modulate the infection pathology and resolution. Innate immune molecules, such as the cytokines interleukin-1 beta and tumor necrosis factor-alpha, fluctuate with the time of day of increased activity and sleep propensity, increase in response to increased waking activity from sleep loss, and are altered from infection by bacteria and viruses to alter sleep and the electroencephalogram. This review focuses innate immune mechanisms of how pathogen recognition receptors, pathogen-associated molecular patterns and danger-associated molecular patterns, energy-related molecules, oxidative stress, and inflammasomes are activated with infection to potentially affect sleep.