The immune proteins — collectively called inflammasome NLRP3 — recruit a sleep-inducing molecule to trigger somnolence following sleep deprivation and exposure to a bacterial toxin, showed results of the study published in the journal Brain, Behavior, and Immunity.
Animals lacking genes for this protective immune complex showed profound sleep aberrations.
“Our research points, for the first time, to the inflammasome acting as a universal sensing mechanism that regulates sleep through the release of immune molecules,” said study senior investigator Mark Zielinski from Harvard Medical School.
In a series of experiments, the scientists demonstrated that following sleep deprivation or exposure to bacteria, the inflammasome activates an inflammatory molecule called interleukin-1 beta, known to induce sleep and promote sleep intensity.
The brain cells of mice lacking the gene coding for inflammasome NLRP3 showed a marked absence of this sleep-inducing molecule.
Going a step further, the investigators compared the behaviour, sleep patterns and electrical activity in the brains of mice lacking the inflammasome gene to those in a group of mice with intact inflammasome genes.
Mice lacking the inflammasome gene had abnormal sleep responses following sleep deprivation.
On average, such mice slept less and experienced more sleep interruptions than mice with their genes intact.
The latter group also slept more and harder following bacterial exposure — the expected physiological response following infection, the researchers said.