Microbial Products and Cytokines in Sleep and Fever Regulation.
Level 5 - mechanism / opinion, no new human data
Narrative review of animal models and mechanistic pathways
PubMed 29773024 · doi:10.1615/CritRevImmunol.v37.i2-6.70
What was done
This narrative review summarizes preclinical and animal research examining sleep architecture and fever responses to systemic infection. It reviews the effects of bacterial, viral, protozoan, and fungal components (such as muramyl peptides, endotoxin, and double-stranded RNA) and specific cytokines on non-rapid eye movement sleep (NREMS), rapid eye movement sleep (REMS), and downstream signaling pathways involving growth hormone-releasing hormone (GHRH) and nitric oxide (NO).
What was found
The abstract reports no quantitative metrics or effect sizes. Qualitatively, infectious challenges in animal models typically induce an initial robust increase in NREMS followed by NREMS inhibition, alongside REMS suppression. Specific cytokines (interleukin-1, tumor necrosis factor, acidic fibroblast growth factor, interferon-alpha) are somnogenic when administered centrally or intravenously, whereas others (interleukin-2, interleukin-6, interferon-beta, basic fibroblast growth factor) lack somnogenic effects. Anti-GHRH or NO production inhibitors block baseline sleep and interleukin-1-induced sleep.
Why it matters
This review outlines the molecular and cytokine mechanisms by which innate immune activation regulates sleep architecture during infection, characterizing sleep alteration as an active component of host defense.
Limits
The abstract describes a narrative review of animal and mechanistic studies without reporting quantitative data, search methodology, or sample sizes. Clinical applicability and direct human physiological data were not assessed.
Cited by
- supports Infecting an animal produces an immune antibody response and a cytokine cascade involving TNF-alpha, IL-1, and IL-6 that directly signals the hypothalamus to trigger sleep.