HEALTH AND WELL-BEING
a sample of the general population, people reported that even modest nightly changes in sleep quality result in day-to-day changes in experienced pain; decreased sleep was linked to increased responsivity to pain and vice versa. The team suggests improving sleep quality, especially in hospital settings, could be an effective approach for pain management.
Fighting infection Other research has directly linked sleep to the immune system, explaining why people may sleep more when they are ill. In a study of over 12,000 lines of fruit flies, researchers from Amita Sehgal’s group in the Perelman School of Medicine at the University of Pennsylvania, US, found that a single gene increases the need for sleep.4 The gene regulates an antimicrobial peptide called Nemuri which is secreted by cells in the brain and drives prolonged, deep sleep after an infection. Flies bred without the Nemuri
gene woke more easily during daily sleep, and were less likely to sleep more even when they were sleep- deprived or fighting an infection. In flies with the Nemuri gene, sleep deprivation stimulated protein expression in a small group of neurons close to a known sleep- promoting structure in the brain. Flies that were infected with bacteria slept more and were more likely to survive if they had the Nemuri gene. The researchers say that infection
appears to trigger Nemuri to fight off microbes, and to increase sleep by acting on the brain. They suggest that this apparent sleep-promoting role may be just as important for health, given that the flies that slept more during sickness had higher survival rates. ‘The Nemuri protein is a genuine
driver of keeping sleep on track under conditions of high sleep need, like when we’re sick,’ says first author Hirofumi Toda, a postdoctoral fellow. ‘In the next phase of our work, we plan to investigate the mechanism by which Nemuri drives sleep.’ Meanwhile, researchers in
Germany have discovered how sleep can help fight infection, whereas other conditions, such as chronic stress, can make the body more susceptible. Stoyan Dimitrov and
We don’t know yet whether getting adequate sleep as people age will protect against Alzheimer’s. But it can’t hurt, and these and other data suggest that it may even help delay and slow down the disease process if it has begun.
David Holtzman Washington University
receptor agonists, sleep improves the potential ability of T cells to attach to their targets. So sleep is good for the immune system, they say, and chronic stress is not.
‘Our findings show that sleep has the potential to enhance the efficiency of T cell responses, which is especially relevant in light of the high prevalence of sleep disorders and conditions characterised by impaired sleep, such as depression, chronic stress, ageing and shift work,’ says Besedovsky.
Luciana Besedovsky, at the University of Tübingen, studied T-cells, a type of white blood cell. To work effectively, T-cells need
In a study of over 12,000 lines of fruit flies, researchers found that a single gene increases the need for sleep. The gene regulates an antimicrobial peptide called Nemuri which is secreted by cells in the brain and drives prolonged, deep sleep after an infection.
DNA damage has been shown in zebra fish to build up during wakefulness while, at the same time, DNA maintenance - chromosome dynamics - is sluggish. However, when the fish slept, chromosome dynamics increased.
to latch on tightly to their targets. This involves activation of a set of receptors (β2-integrins), which span the cell membrane and encourage adhesion. The German team found that certain molecules called Gαs- coupled receptor agonists, including the hormones adrenaline and noradrenaline, the pro-inflammatory molecules prostaglandin E2 and D2, and the neuromodulator adenosine, prevented T cells from activating their integrins. ‘The levels of [Gαs-coupled
receptor agonists] needed to inhibit integrin activation are increased in many pathological conditions, such as tumour growth, malaria infection, hypoxia, and stress,’ says Dimitrov. ‘This pathway may therefore contribute to the immune suppression associated with these pathologies.’ It’s known that adrenaline and
prostaglandin levels dip during sleep. The team compared T cells taken from healthy volunteers while they slept or were awake all night. Those taken from sleeping volunteers showed significantly higher levels of integrin activation than those taken from wakeful subjects. The researchers say that, by lowering levels of Gαs-coupled
DNA repair Sleep is also a time for the body to repair DNA damage, according to a recent study on nerve cells (neurons) from Bar-Ilan University in Israel. Many processes, such as radiation, oxidative stress and even neuronal activity, can cause DNA damage, but each cell has a repair system to correct this damage. The team studied this system in zebrafish.5 Using a high-resolution
microscope and 3D time-lapse imaging techniques, the team studied single cells, which are transparent. They were able to observe the movement of DNA and nuclear proteins within the cell while the fish were awake and asleep. In this way, they showed that DNA damage builds up and can reach unsafe levels during wakefulness; at the same time, DNA maintenance (chromosome dynamics) is sluggish. However, when the fish slept, chromosome dynamics increased. ‘It’s like potholes in the road,’ says
team leader Lior Appelbaum. ‘Roads accumulate wear and tear, especially during daytime rush hours, and it is most convenient and efficient to fix them at night, when there is light traffic.’ Appelbaum calls the build-up of DNA damage the ‘price of wakefulness’. ‘We’ve found a causal link between
sleep, chromosome dynamics, neuronal activity, and DNA damage and repair with direct physiological relevance to the entire organism,’ he says. ‘Sleep gives an opportunity to reduce DNA damage accumulated in the brain during wakefulness. Despite the risk of reduced awareness to the environment, animals have to sleep to allow their neurons to perform efficient DNA maintenance, and this is possibly the reason why sleep has evolved and is so conserved in the
28 06 | 2019
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