Intelligence  

New research shows that infections can impair cognitive ability measured on an IQ scale. The study is the largest of its kind to date, and it shows a clear correlation between infection levels and impaired cognition.

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nyone can suffer from an infection, for example in their stomach, urinary tract or skin. However, a new Danish study shows that a patient’s distress does not necessarily end once the infection has been treated. In fact, ensuing infections can affect your cognitive ability measured by an IQ test:

“Our research shows a correlation between hospitalization due to infection and impaired cognition corresponding to an IQ score of 1.76 lower than the average. People with five or more hospital contacts with infections had an IQ score of 9.44 lower than the average. The study thus shows a clear dose-response relationship between the number of infections, and the effect on cognitive ability increased with the temporal proximity of the last infection and with the severity of the infection. Infections in the brain affected the cognitive ability the most, but many other types of infections severe enough to require hospitalization can also impair a patient’s cognitive ability. Moreover, it seems that the immune system itself can affect the brain to such an extent that the person’s cognitive ability measured by an IQ test will also be impaired many years after the infection has been cured,” explains MD and PhD Michael Eriksen Benrós, who is affiliated with the National Centre for Register-Based Research at Aarhus BSS and the Mental Health Centre Copenhagen, University of Copenhagen.

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He has conducted the research in collaboration with researchers from the University of Copenhagen and Aarhus University. 190,000 Danes participated in the study who have had their IQ assessed between 2006 and 2012. 35% of these individuals had a hospital contact with infections before the IQ testing was conducted.

According to Benrós, part of the explanation of the increased risk of impaired cognition following an infection may be as follows:

“Infections can affect the brain directly, but also through peripheral inflammation, which affects the brain and our mental capacity. Infections have previously been associated with both depression and schizophrenia, and it has also been proven to affect the cognitive ability of patients suffering from dementia. This is the first major study to suggest that infections can also affect the brain and the cognitive ability in healthy individuals.”

"This is the first major study to suggest that infections can also affect the brain and the cognitive ability in healthy individuals."

“We can see that the brain is affected by all types of infections. Therefore, it is important that more research is conducted into the mechanisms which lie behind the connection between a person’s immune system and mental health,” says Benrós.

He hopes that learning more about this connection will help to prevent the impairment of people’s mental health and improve future treatment.

Experiments on animals have previously shown that the immune system can affect cognitive capabilities, and more recent minor studies in humans have also pointed in that direction. Normally, the brain is protected from the immune system, but with infections and inflammation the brain may be affected. Benrós’ research suggests that it may be the immune system that causes the cognitive impairment, not just the infection, because many different types of infections were associated with a decrease in cognitive abilities.

This is the first study to examine these correlations in this manner. The results suggest that the immune system’s response to infections can possibly affect the brain and thereby also the person’s cognitive ability. This is in line with previous studies, some of which have also been conducted by Benrós, which show that infections are associated with an increased risk of developing mental disorders such as depression or schizophrenia.

The researchers behind the study hope that their results may spur on further research on the possible involvement of the pin the development of psychiatric disorders and whether the discovered correlations contribute to the development of mental disorders or whether they may be caused by e.g. genetic liability toward acquiring infections in patients with reduced cognitive ability. The study has been adjusted for social conditions and parental educational levels; however, it cannot be ruled out that heritable and environmental factors associated with infections might also influence the associations.


SOURCE  Aarhus University

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 Medicine  

When we get sick it feels natural to try to hasten our recovery by getting some extra sleep. Researchers have found that this response has a definite purpose, in fruit flies: enhancing immune system response and recovery to infection.

When we get sick it feels natural to try to hasten our recovery by getting some extra sleep.  Now researchers from the Perelman School of Medicine at the University of Pennsylvania have found that this response has a definite purpose.  They found that in fruitflies sleep enhances immune system response and recovery to infection.

The findings appear online in two related papers in the journal Sleep, in advance of print editions in May and June.

Unexpectedly, the pre-infection, sleep-deprived flies had a better survival rate.

"It's an intuitive response to want to sleep when you get sick," notes Center for Sleep and Circadian Neurobiology research associate Julie A. Williams, PhD. "Many studies have used sleep deprivation as a means to understand how sleep contributes to recovery, if it does at all, but there is surprisingly little experimental evidence that supports the notion that more sleep helps us to recover. We used a fruitfly model to answer these questions." Along with post-doctoral fellow, Tzu-Hsing Kuo, PhD, Williams conducted two related studies to directly examine the effects of sleep on recovery from and survival after an infection.

In the first paper, they took a conventional approach by subjecting fruit flies to sleep deprivation before infecting them with either Serratia marcescens or Pseudomonas aeruginosa bacteria. Both the sleep-deprived flies and a non-sleep-deprived control group displayed increased sleep after infection, what the experimenters call an "acute sleep response."

Unexpectedly, the pre-infection, sleep-deprived flies had a better survival rate. "To our surprise they actually survived longer after the infection than the ones who were not sleep-deprived," notes Williams. The Penn team found that prior sleep deprivation made the flies sleep for a longer period after infection as compared to the undisturbed controls. They slept longer and they lived longer during the infection.

Inducing sleep deprivation after infection rather than before made little difference, as long as the infected flies then got adequate recovery sleep. "We deprived flies of sleep after infection with the idea that if we blocked this sleep, things would get worse in terms of survival," Williams explains. "Instead they got better, but not until after they had experienced more sleep."

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Sleep deprivation increases activity of an NFkB transcription factor, Relish, which is also needed for fighting infection. Flies without the Relish gene do not experience an acute sleep response and very quickly succumb to infection. But, when these mutants are sleep-deprived before infection, they displayed increased sleep and survival rates after infection. The team then evaluated mutant flies that lacked two varieties of NFkB (Relish and Dif). When flies lacked both types of NFkB genes, sleep deprivation had no effect on the acute sleep response, and the effect on survival was abolished. Flies from both sleep-deprived and undisturbed groups succumbed to infection at equal rates within hours.

"Taken together, all of these data support the idea that post-infection sleep helps to improve survival," Williams says.

In the second study, the researchers manipulated sleep through a genetic approach. They used the drug RU486 to induce expression of ion channels to alter neuronal activity in the mushroom body of the fly brain, and thereby regulate sleep patterns. Compared to a control group, flies that were induced to sleep more, and for longer periods of time for up to two days before infection, showed substantially greater survival rates. The fruit flies with more sleep also showed faster and more efficient rates of clearing the bacteria from their bodies. "Again, increased sleep somehow helps to facilitate the immune response by increasing resistance to infection and survival after infection," notes Williams.

Because the genetic factors investigated by the Penn team, such as the NFkB pathway, are preserved in mammals, the relative simplicity of the Drosophila model provides an ideal avenue to explore basic functions like sleep. "Investigators have been working on questions about sleep and immunity for more than 40 years, but by narrowing down the questions in the fly we're now in a good position to identify potentially novel genes and mechanisms that may be involved in this process that are difficult to see in higher animals," explains Williams.

"These studies provide new evidence of the direct and functional effects of sleep on immune response and of the underlying mechanisms at work. The take-home message from these papers is that when you get sick, you should sleep as much as you can -- we now have the data that supports this idea," she concludes.



SOURCE  University of Pennsylvania via EurekAlert

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 Medicine  

Medical researchers have discovered how the immune system kills healthy cells while attacking infections. Their findings could one day lead to more targeted treatments for cancer and viral infections.

Medical scientists at the University of Alberta have discovered how the immune system kills healthy cells while attacking infections. Their findings could one day lead to better treatments for cancer and viral infections.

Colin Anderson, a researcher with the Faculty of Medicine & Dentistry, recently published his team’s findings in the peer-reviewed Journal of Immunology. His team included colleagues from the United States and the Netherlands, and graduate students from the U of A.

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Previous research has shown that when the immune system launches an aggressive attack on infected cells, healthy tissues and cells can be killed or damaged in the process. Anderson and his team discovered the mechanisms in the immune system that cause this “overkill” response.

“This opens the opportunity that one might be able to manipulate the immune-system response to block collateral damage without blocking the killing of infected cells,” Anderson explained.

“In the future, this might be important in the development of clinical treatments in cases where the immune system response needs to be harnessed. For example, in treating various viral infections, the collateral damage caused during the immune-system attack is a large part of the illness.

“In other cases, such as cancer or tumour treatments, one may want to increase the immune system’s ability to kill collateral cells, in hopes of killing tumour cells that would otherwise escape during treatment and spread elsewhere in the body. Our research suggests there are other mechanisms that could improve cancer therapy and make it more efficacious. This finding could also help us understand why certain cancer treatments are more successful than others.”

Anderson’s team discovered that “the weaponry the immune system uses to try to kill an infected or cancerous cell is not exactly the same as the weaponry that causes collateral damage to innocent bystander cells that aren’t infected.” For years, it was assumed the weaponry to kill infected cells versus healthy cells was exactly the same.

The research group is continuing work in this area to see whether they can alter the level of collateral damage to healthy cells without altering the attack on infected cells.

Anderson is a researcher in the Department of Surgery and the Department of Medical Microbiology and Immunology. He is also a member of the Alberta Diabetes Institute and the Alberta Transplant Institute.



SOURCE  University of Alberta

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 Medicine  

A research team at San Diego State University has found a previously unidentified immune system that protects humans and animals from infection in mucous.

Mucous may be slimy and gross, and the source of embarrassment and jokes, but a San Diego State University research team, led by Biology Post-doctoral Fellow Jeremy Barr, has discovered that it is also home to a powerful immune system that could change the way doctors treat a number of diseases.

In this previously undocumented immune system, researchers uncovered bacteria-infecting viruses known as bacteriophage, which shield the body from invading infection.

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The discovery, made possible with funding from the National Institutes of Health, concentrates on the protective layers of mucus which are present in all humans and animals. It serves both as a home for large populations of beneficial microbes — which can include fungi, bacteria and viruses — and as an entry point for infection.

The research was published in the May Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS).

The researchers sampled mucous from animals and humans — ranging from a sea anemone to a mouse and a person — and found that bacteriophage adheres to the mucus layer on all of them.

They placed bacteriophage on top of a layer of mucus-producing tissue and observed that the bacteriophage formed bonds with sugars within the mucus, causing them to adhere to the surface. They then challenged these mucus cells with E. coli bacteria and found that the bacteriophage attacked and killed off the E. coli in the mucus, effectively forming an anti-microbial barrier on the host that protected it from infection and disease.

Researcher Jeremy Barr

To confirm their discovery, the team also conducted parallel research challenging non-mucus producing cells with both bacteriophage and E. coli. The results — the samples with no mucus had three times more cell death.

“Taking previous research into consideration, we are able to propose the Bacteriophage Adherence to Mucus — or BAM — is a new model of immunity, which emphasizes the important role bacteriophage play in protecting the body from invading pathogens,” Barr said.

According to Barr, part of what makes this research so novel is that bacteriophage are already present on all humans and animals.

The body recruits the bacteriophage from the environment, which then naturally sticks to mucus layers across various parts of the body including the mouth and gut. The bacteriophage then becomes a protector of its host, accumulating and attacking on its own.

“This discovery not only proposes a new immune system but also demonstrates the first symbiotic relationship between phage and animals,” Barr said. “It will have a significant impact across numerous fields.”

“The research could be applied to any mucosal surface,” Barr said. “We envision BAM influencing the prevention and treatment of mucosal infections seen in the gut and lungs, having applications for phage therapy and even directly interacting with the human immune system.”


SOURCE  San Diego State University

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