Milky Way not unusual, astronomers find

The first detailed cross-section of a galaxy broadly similar to the Milky Way, published today, reveals that our galaxy evolved gradually, instead of being the result of a violent mash-up. The finding throws the origin story of our home into doubt.

The galaxy, dubbed UGC 10738, turns out to have distinct 'thick' and 'thin' discs similar to those of the Milky Way. This suggests, contrary to previous theories, that such structures are not the result of a rare long-ago collision with a smaller galaxy. They appear to be the product of more peaceful change.

And that is a game-changer. It means that our spiral galaxy home isn't the product of a freak accident. Instead, it is typical.

The finding was made by a team led by Nicholas Scott and Jesse van de Sande, from Australia's ARC Centre of Excellence for All Sky Astrophysics in 3 Dimensions (ASTRO 3D) and the University of Sydney.

"Our observations indicate that the Milky Way's thin and thick discs didn't come about because of a gigantic mash-up, but a sort-of 'default' path of galaxy formation and evolution," said Dr Scott.

"From these results we think galaxies with the Milky Way's particular structures and properties could be described as the 'normal' ones."

This conclusion -- published in The Astrophysical Journal Letters- has two profound implications.

"It was thought that the Milky Way's thin and thick discs formed after a rare violent merger, and so probably wouldn't be found in other spiral galaxies," said Dr Scott.

"Our research shows that's probably wrong, and it evolved 'naturally' without catastrophic interventions. This means Milky Way-type galaxies are probably very common.

"It also means we can use existing very detailed observations of the Milky Way as tools to better analyse much more distant galaxies which, for obvious reasons, we can't see as well."

The research shows that UGC 10738, like the Milky Way, has a thick disc consisting mainly of ancient stars -- identified by their low ratio of iron to hydrogen and helium. Its thin disc stars are more recent and contain more metal.

(The Sun is a thin disc star and comprises about 1.5% elements heavier than helium. Thick disc stars have three to 10 times less.)

Although such discs have been previously observed in other galaxies, it was impossible to tell whether they hosted the same type of star distribution -- and therefore similar origins. Scott, van de Sande and colleagues solved this problem by using the European Southern Observatory's Very Large Telescope in Chile to observe UGC 10738, situated 320 million light years away.

The galaxy is angled "edge on," so looking at it offered effectively a cross-section of its structure.

"Using an instrument called the multi-unit spectroscopic explorer, or MUSE, we were able to assess the metal ratios of the stars in its thick and thin discs," explained Dr van de Sande.

"They were pretty much the same as those in the Milky Way -- ancient stars in the thick disc, younger stars in the thin one. We're looking at some other galaxies to make sure, but that's pretty strong evidence that the two galaxies evolved in the same way."

Dr Scott said UGC 10738's edge-on orientation meant it was simple to see which type of stars were in each disc.

"It's a bit like telling apart short people from tall people," he said. "It you try to do it from overhead it's impossible, but it if you look from the side it's relatively easy."

Co-author Professor Ken Freeman from the Australian National University said, "This is an important step forward in understanding how disk galaxies assembled long ago. We know a lot about how the Milky Way formed, but there was always the worry that the Milky Way is not a typical spiral galaxy. Now we can see that the Milky Way's formation is fairly typical of how other disk galaxies were assembled."

ASTRO 3D director, Professor Lisa Kewley, added: "This work shows how the Milky Way fits into the much bigger puzzle of how spiral galaxies formed across 13 billion years of cosmic time."

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Press (re)play to remember - How the brain strengthens memories during sleep

While we sleep, the brain produces particular activation patterns. When two of these patterns -- slow oscillations and sleep spindles -- gear into each other, previous experiences are reactivated. The stronger the reactivation, the clearer will be our recall of past events, a new study reveals.

Scientists have long known that slow oscillations (SOs) and sleep spindles -- sudden half-second to two-second bursts of oscillatory brain activity -- play an important role in the formation and retention of new memories.

But experts in the UK and Germany have discovered that the precise combination of SOs and sleep spindles is vital for opening windows during which memories are reactivated; helping to form and cement memories in the human brain.

Researchers at the University of Birmingham and Ludwig-Maximilians-University Munich today published their findings in Nature Communications.

Co-author Dr Bernhard Staresina, from the University of Birmingham's School of Psychology, commented: "Our main means of strengthening memories while we sleep is the reactivation of previously learnt information, which allows us to solidify memories in neocortical long-term stores.

"We have discovered an intricate interplay of brain activity -- slow oscillations and sleep spindles -- which create windows of opportunity enabling this reactivation."

Co-author Dr Thomas Schreiner, from Ludwig-Maximilians-University, Munich, commented: "Memory reactivation is specifically bound to the presence of SO-spindle complexes. These results shed new light on the memory function of sleep in humans and emphasise the importance of orchestrated sleep rhythms in strengthening our powers of recall and orchestrating the creation of memories."

Before this study, evidence of the brain's capacity to reactivate memories during sleep was scarce, but the team devised novel tests where participants were shown information before taking a nap and closely monitored brain activity during non-rapid eye movement (NREM) sleep using EEG recording. Those taking part were then tested on their memory recall after waking up, allowing the researchers to link the extent of memory reactivation during sleep to memory performance.

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Narcissism linked to aggression in review of 437 studies

A comprehensive analysis of 437 studies from around the world provides the best evidence to date that narcissism is an important risk factor for both aggression and violence, researchers said.

The link between narcissism and aggression was found for all dimensions of narcissism and for a variety of types of aggression. Results were similar regardless of gender, age, whether they were college students, or country of residence.

And, to have an impact, narcissism doesn't have to be at levels so high as to be pathological. Findings showed that even when narcissism was within what is considered a normal range, higher levels were linked to aggression.

"It is a pretty straightforward message: Narcissism is a significant risk factor for aggressive and violent behavior across the board," said Brad Bushman, co-author of the study and professor of communication at The Ohio State University.

The study was led by Sophie Kjaervik, a graduate student in communication at Ohio State. It was published yesterday (May 24, 2021) in the journal Psychological Bulletin.

"The link we found between narcissism and aggression was significant -- it was not trivial in size," Kjaervik said. "The findings have important real-world implications."

The researchers combined and analyzed data from many studies to provide a comprehensive view of this research area. In this meta-analysis, they examined data from 437 independent studies with a total of 123,043 participants.

Narcissism is characterized by an overblown sense of self-importance, Bushman said. The key component of narcissism is entitlement. Narcissism also has two peripheral components: grandiose (those with high self-esteem) and vulnerable (those with low self-esteem). The study found all of these components were linked to aggression.

Narcissism was related to all forms of aggression measured in the studies the researchers analyzed, including physical, verbal, bullying, direct or indirect, and displaced onto innocent targets.

"Individuals who are high in narcissism are not particularly picky when it comes to how they attack others," Kjaervik said.

Findings showed that narcissism was linked to online cyberbullying, as well as bullying offline.

"That's a highly important finding now that we live in an online world," she said.

People higher in narcissism were not only more likely to lash out in anger, but were also more likely to be "cold, deliberate and proactive" in their aggression, Bushman said.

People high in narcissism were more likely than others to be aggressive whether they were provoked or not, the study found. But the risk for aggression was significantly higher when they felt provoked, such as being ignored or insulted.

The researchers were somewhat surprised to find that the link between narcissism and violence was nearly as strong as its link with less serious forms of aggression. Violence is more rare than and is generally more difficult to predict than lesser forms of aggression, Bushman said. In this study, violence was defined as aggression intended to cause physical harm such as injury or death.

But these results are consistent with research suggesting that narcissism might be a risk factor for extremely violent acts such as mass shootings, he said.

One argument could be that the narcissism-aggression link would be more likely to occur in individualistic countries, like the United States, where people emphasize their personal rights. But the analysis found that narcissism and aggression were related even in more collectivist countries.

And findings were similar whether the research participants were college students or a more general population.

It might be tempting to think these results apply only to people who are "narcissists," but that would be wrong, Bushman said.

For one, you can't separate people into those who are narcissists and those who are not. Nearly everyone has some degree of narcissism, even though only a minority have levels high enough to be called pathological.

Findings in this study suggest that higher levels of narcissism are related to more aggression even before it reaches pathological levels.

"All of us are prone to being more aggressive when we are more narcissistic," Bushman said.

One thing that clearly stood out in the analysis, he said, was how people high in narcissism respond when they feel threatened.

"Our results suggest provocation is a key moderator of the link between narcissism and aggression," Bushman said.

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Immune cells imperfect at distinguishing between friend and foe

When it comes to distinguishing a healthy cell from an infected one that needs to be destroyed, the immune system's killer T cells sometimes make mistakes.

This discovery, described today in eLife, upends a long-held belief among scientists that T cells were nearly perfect at discriminating friend from foe. The results may point to new ways to treat autoimmune diseases that cause the immune system to attack the body, or lead to improvements in cutting-edge cancer treatments.

It is widely believed that T cells can discriminate perfectly between infected cells and healthy ones based on how tightly they are able to bind to molecules called antigens on the surface of each. They bind tightly to antigens derived from viruses or bacteria, but less tightly to our own antigens on normal cells. But recent studies by scientists looking at autoimmune diseases suggest that T cells can attack otherwise normal cells if they express unusually large numbers of our own antigens, even though these bind only weakly.

"We set out to resolve this discrepancy between the idea that T cells are near perfect at discriminating between healthy and infected cells based on the antigen binding strength, and clinical results that suggests otherwise," says co-first author Johannes Pettmann, a D.Phil student at the Sir William Dunn School of Pathology and Radcliffe Department of Medicine, University of Oxford, UK. "We did this by very precisely measuring the binding strength of different antigens."

The team measured exactly how tightly receptors on T cells bind to a large number of different antigens, and then measured how T cells from healthy humans responded to cells loaded with different amounts of these antigens. "Our methods, combined with computer modelling, showed that the T cell's receptors were better at discrimination compared to other types of receptors," says co-first author Anna Huhn, also a D.Phil student at the Sir William Dunn School of Pathology, University of Oxford. "But they weren't perfect -- their receptors compelled T cells to respond even to antigens that showed only weak binding."

"This finding completely changes how we view T cells," adds Enas Abu-Shah, Postdoctoral Fellow at the Kennedy Institute and the Sir William Dunn School of Pathology, University of Oxford, and also a co-first author of the study. "Instead of thinking of them as near-perfect discriminators of the antigen binding strength, we now know that they can respond to normal cells that simply have more of our own weakly binding antigens."

The authors say that technical issues with measuring the strength of T cell receptor binding in previous studies likely led to the mistaken conclusion that T cells are perfect discriminators, highlighting the importance of using more precise measurements.

"Our work suggests that T cells might begin to attack healthy cells if those cells produce abnormally high numbers of antigens," says senior author Omer Dushek, Associate Professor at the Sir William Dunn School of Pathology, University of Oxford, and a Senior Research Fellow in Basic Biomedical Sciences at the Wellcome Trust, UK. "This contributes to a major paradigm shift in how we think about autoimmunity, because instead of focusing on defects in how T cells discriminate between antigens, it suggests that abnormally high levels of our own antigens may be responsible for the mistaken autoimmune T-cell response. On the other hand, this ability could be helpful to kill cancer cells that mutate to express abnormally high levels of our antigens."

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36 dwarf galaxies had simultaneous 'baby boom' of new stars

Three dozen dwarf galaxies far from each other had a simultaneous "baby boom" of new stars, an unexpected discovery that challenges current theories on how galaxies grow and may enhance our understanding of the universe.

Galaxies more than 1 million light-years apart should have completely independent lives in terms of when they give birth to new stars. But galaxies separated by up to 13 million light-years slowed down and then simultaneously accelerated their birth rate of stars, according to a Rutgers-led study published in the Astrophysical Journal.

"It appears that these galaxies are responding to a large-scale change in their environment in the same way a good economy can spur a baby boom," said lead author Charlotte Olsen, a doctoral student in the Department of Physics and Astronomy in the School of Arts and Sciences at Rutgers University-New Brunswick.

"We found that regardless of whether these galaxies were next-door neighbors or not, they stopped and then started forming new stars at the same time, as if they'd all influenced each other through some extra-galactic social network," said co-author Eric Gawiser, a professor in the Department of Physics and Astronomy.

The simultaneous decrease in the stellar birth rate in the 36 dwarf galaxies began 6 billion years ago, and the increase began 3 billion years ago. Understanding how galaxies evolve requires untangling the many processes that affect them over their lifetimes (billions of years). Star formation is one of the most fundamental processes. The stellar birth rate can increase when galaxies collide or interact, and galaxies can stop making new stars if the gas (mostly hydrogen) that makes stars is lost.

Star formation histories can paint a rich record of environmental conditions as a galaxy "grew up." Dwarf galaxies are the most common but least massive type of galaxies in the universe, and they are especially sensitive to the effects of their surrounding environment.

The 36 dwarf galaxies included a diverse array of environments at distances as far as 13 million light-years from the Milky Way. The environmental change the galaxies apparently responded to must be something that distributes fuel for galaxies very far apart. That could mean encountering a huge cloud of gas, for example, or a phenomenon in the universe we don't yet know about, according to Olsen.

The scientists used two methods to compare star formation histories. One uses light from individual stars within galaxies; the other uses the light of a whole galaxy, including a broad range of colors.

"The full impact of the discovery is not yet known as it remains to be seen how much our current models of galaxy growth need to be modified to understand this surprise," Gawiser said. "If the result cannot be explained within our current understanding of cosmology, that would be a huge implication, but we have to give the theorists a chance to read our paper and respond with their own research advances."

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Explanation of how religious beliefs may be formed

Feeling anxious can direct our attention and memory toward supernatural beings such as gods, a University of Otago study has found.

Lead author Dr Thomas Swan, of the Department of Psychology, says the research may help explain how religious beliefs are formed.

For the study, published in the International Journal for the Psychology of Religion, 972 participants completed an online recall test to determine if a bias to recall supernatural agents was stronger in anxious people, rather than non-anxious people.

Those who felt anxious were more likely to remember beings with supernatural abilities than beings without.

"Anxiety is an emotion that evolved to make us pay greater attention to potential threats, so when we feel anxious, a god that can read our thoughts and punish us for them, or flood the Earth, is going to be memorable," he says.

Previous research has shown anxiety can lead to greater levels of religious belief, with the explanation being that belief provides comfort. However, this so-called 'comfort theory' has problems: why are there punishing gods and hellish afterlives when these are far from comforting?

Dr Swan believes the theory also fails to address what comes between feeling anxious and becoming a believer. This research suggests the first step involves the cognitive effects of anxiety, which cause people to attend to and recall threats.

"In our previous research, we found that supernatural beings are perceived as potentially threatening because they have abilities that defy our expectations about the world. The present research confirms that the cognitive effects of anxiety also extend to the threat that is afforded by supernatural beings.

"Ironically then, our research suggests comfort theory has it somewhat backwards: anxious people are attracted, at least initially, to the scary traits of gods, which may explain why so many gods have scary features. Comfort, we suspect, comes later when some people transform their view of the god into something more palatable that they are happier believing," he says.

The research also suggests other supernatural concepts -- such as ghosts, psychics, and astrology -- will be digested in the same way because of how they alarmingly defy our expectations about what is possible.

Dr Swan hopes the research prompts people to develop a greater understanding of how their emotional states affect the information they look at and remember, particularly religious information.

"We should all be mindful of how we came to believe the things we do, especially those with anxiety disorders who feel anxious much of the time -- they should be mindful of what they are attracted to and why. If they find themselves reading fantasy novels, that may be harmless. If they find themselves joining a cult, then it's time for some reflection. The same goes for people without disorders who are just in anxious situations, such as sitting in a hospital bed or suffering financial troubles."

On the flipside, he hopes religious groups pay more attention to people's mental states.

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Digital Twin technology a 'powerful tool' but requires significant investment, say experts

Healthcare and aerospace experts at King's College London, The Alan Turing Institute, the University of Cambridge, and the Oden Institute for Computational Engineering and Sciences at UT Austin in Texas have said advances in digital twin technology make it a powerful tool for facilitating predictive and precision medicine and enhancing decision-making for aerospace systems. Their opinion piece was published today in Nature Computational Science.

When applied to healthcare, the digital twin, a virtual version of real-life objects that can be used to predict how that object will perform, could predict how a patient's disease will develop and how patients are likely to respond to different therapies.

It is also of huge benefit in aerospace, where, for example, the technology will be needed to monitor and control thousands of drones, ensuring that they are maintained, have efficient and safe flight plans and can automatically adapt to changes in conditions, such as weather, without the need for human interaction.

However, current digital twins are largely the result of bespoke technical solutions that are difficult to scale.

The authors say that these use cases place new demands on the speed, robustness, validation, verification and uncertainty quantification in digital twin creation workflows.

Achieving digital twins at scale will require a drastic reduction in technical barriers to their adoption.

Lead author Professor Steven Niederer from the School of Biomedical Engineering & Imaging Sciences, King's College London said in medicine, the digital twin will allow testing of a large number of therapies on a patient to identify the best option for that individual with their unique disease.

"There is, however, a need to invest in the underlying theory for how to make models, how to run these models at speed and how to combine multiple models together to ensure that they run as expected," he said.

"We also need to further develop the mathematics of how we create digital twins from patient data, how we measure uncertainty in patient data, and how to account for uncertainty in the model in predictions. These are all things which need further investment."

"We are making more measurements in patients in the hospital and from remote monitoring and we need to develop methods for rapidly and robustly combining this patient information into a digital twin to provide a single representation of the patient."

"Another challenge is how do we get better at predicting how the heart will operate under extreme conditions. We often want to predict when the heart will fail, however, we only have information that is obtained from them under normal operating procedures."

Similarly from an aerospace perspective, Dr Karen Willcox, Director, Oden Institute for Computational Engineering and Sciences at The University of Texas at Austin, said in order to be useful, the digital twin must be predictive and quantify uncertainty.

"Digital twins must be able to analyze 'what if' scenarios and issue predictions about the future, in order to guide decision making to manage a physical asset. That means the digital twin cannot be built on data alone, it needs to include both data and predictive models," she said.

Though open challenges remain, the value of digital twins is clear. And they don't have to be perfect to be valuable. "Even with existing limitations, digital twins are providing valuable decision support in many different application areas," said Willcox. "Ultimately we would like to see the technology used in every engineering system. At that point we can start thinking not just about how a digital twin might change the way we operate the system, but also how we design it in the first place."

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Diabetes vaccine gives promising results in a genetic subgroup

A clinical study led by Linköping University and financed by pharmaceuticals company Diamyd Medical has investigated whether immunotherapy against type 1 diabetes can preserve the body's own production of insulin. The results suggest that injection of a protein, GAD, into lymph nodes can be effective in a subgroup of individuals. The results have been published in Diabetes Care.

In type 1 diabetes, the body's immune system attacks the cells that produce insulin. When the insulin-producing cells have disappeared, the body can no longer regulate blood sugar level, and a person with type 1 diabetes must take exogenous insulin for the rest of his or her life.

A highly topical question in research into type 1 diabetes is whether, and if so how, the attack of the immune system can be slowed or even completely stopped. One possible strategy is based on altering the immune defence by injecting a protein that the cells of the immune system react to, in a form of vaccination. One of the proteins against which the immune system often forms antibodies in type 1 diabetes is known as GAD65 (glutamic acid decarboxylase). Professor Johnny Ludvigsson at Linköping University has studied for many years the possibility of vaccinating people who have newly diagnosed type 1 diabetes with GAD. It is hoped that the immune system will become more tolerant against the body's own GAD, and stop damaging the insulin-producing cells, such that the body can continue to form some insulin.

"Studies have shown that even an extremely small production of insulin in the body is highly beneficial for patient health. People with diabetes who produce a certain amount of insulin naturally do not develop low blood sugar levels, hypoglycaemia, so easily. They have also a lower risk of developing the life-threatening condition ketoacidosis, which can arise when the insulin level is low," says Johnny Ludvigsson, senior professor in the Department of Biomedical and Clinical Sciences at Linköping University.

Johnny Ludvigsson has led DIAGNODE-2, a clinical phase 2 study in which researchers investigated the effect of GAD-alum (Diamyd) injections into the lymph nodes of 109 young people with recently diagnosed type 1 diabetes. The natural insulin production of the participants was measured at the start of the study and again after 15 months. Several other outcome measures were also followed, such as change in long-term blood sugar levels (HbA1c), and how much supplementary insulin the patients needed to take every day.

Previous studies of immunotherapy in diabetes have suggested that genetic factors play a role in how patients respond to the treatment. This led the researchers in DIAGNODE-2 to look at several variants of what are known as "HLA genes." These genes code for proteins located on the surface of some cells. They function as holders of proteins, and expose them to immune system cells passing by. If the protein fragment exposed in this way comes from, for example, bacteria, the immune system should form antibodies against the foreign protein. However, the immune system sometimes reacts against the body's own substances, and certain types of HLA are associated with an increased risk of type 1 diabetes. The HLA variant HLA-DR3-DQ2 exposes the GAD65 protein to cells of the immune system, and patients with this variant often form antibodies against GAD65 at an early stage of the disease. Around half of the participants in the study had the HLA-DR3-DQ2 variant.

For the complete patient group, there was no difference between treatment and placebo in the degree to which insulin production was preserved. GAD-alum did, however, have a positive effect for the subgroup of patients who had the DR3-DQ2 variant of HLA genes.

"The patients in the subgroup with the DR3-DQ2 type of HLA genes did not lose insulin production as quickly as the other patients. In contrast, we did not see any significant effect in the patients who did not have this HLA type," says Johnny Ludvigsson.

No undesired effects that could be related to treatment with GAD-alum were seen during the study.

"Treatment with GAD-alum seems to be a promising, simple and safe way to preserve insulin production in around half of patients with type 1 diabetes, the ones who have the right type of HLA. This is why we are looking forward to carrying out larger studies, and we hope these will lead to a drug that can change the progress of type 1 diabetes," says Johnny Ludvigsson.

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Origins of life researchers develop a new ecological biosignature

When scientists hunt for life, they often look for biosignatures, chemicals or phenomena that indicate the existence of present or past life. Yet it isn't necessarily the case that the signs of life on Earth are signs of life in other planetary environments. How do we find life in systems that do not resemble ours?

In groundbreaking new work, a team* led by Santa Fe Institute Professor Chris Kempes has developed a new ecological biosignature that could help scientists detect life in vastly different environments. Their work appears as part of a special issue of the Bulletin of Mathematical Biology collected in honor of renowned mathematical biologist James D. Murray.

The new research takes its starting point from the idea that stoichiometry, or chemical ratios, can serve as biosignatures. Since "living systems display strikingly consistent ratios in their chemical make-up," Kempes explains, "we can use stoichiometry to help us detect life." Yet, as SFI Science Board member and contributor, Simon Levin, explains, "the particular elemental ratios we see on Earth are the result of the particular conditions here, and a particular set of macromolecules like proteins and ribosomes, which have their own stoichiometry." How can these elemental ratios be generalized beyond the life that we observe on our own planet?

The group solved this problem by building on two lawlike patterns, two scaling laws, that are entangled in elemental ratios we have observed on Earth. The first of these is that in individual cells, stoichiometry varies with cell size. In bacteria, for example, as cell size increases, protein concentrations decrease, and RNA concentrations increase. The second is that the abundance of cells in a given environment follows a power-law distribution. The third, which follows from integrating the first and second into a simple ecological model, is that the elemental abundance of particles to the elemental abundance in the environmental fluid is a function of particle size.

While the first of these (that elemental ratios shift with particle size) makes for a chemical biosignature, it is the third finding that makes for the new ecological biosignature. If we think of biosignatures not simply in terms of single chemicals or particles, and instead take account of the fluids in which particles appear, we see that the chemical abundances of living systems manifest themselves in mathematical ratios between the particle and environment. These general mathematical patterns may show up in coupled systems that differ significantly from Earth.

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Superficial relationship: Enzymes protect the skin by ignoring microbes and viruses

The human body is constantly exposed to various environmental actors, from viruses to bacteria to fungi, but most of these microbial organisms provoke little or no response from our skin, which is charged with monitoring and protecting from external dangers.

Until now, researchers weren't quite sure how that happened -- and why our skin wasn't constantly alarmed and inflamed.

In a study published May 21, 2021 in Science Immunology, scientists at University of California San Diego School of Medicine identify and describe two enzymes responsible for protecting our skin and body's overall health from countless potential microbial intruders. These enzymes, called histone deacetylases (HDACs), inhibit the body's inflammatory response in the skin.

"We have figured out why we tolerate certain microbes living on our skin, while the same bacteria would make us very sick if exposed elsewhere in the body," said Richard Gallo, MD, PhD, Ima Gigli Distinguished Professor of Dermatology and chair of the Department of Dermatology at UC San Diego School of Medicine. "In our research, we identified enzymes that act on the chromosome of specific skin cells that provide immune tolerance by the skin.

"Without these enzymes telling our cells to ignore certain bacteria, we'd have a constant rash on our skin."

Gallo and colleagues say the potential mechanism for how the environment can interact and alter cell function is through epigenetic control of gene expression. Within the skin cells, proteins called toll-like receptors (TLRs) allow the cells to sense their surroundings and potential dangers.

In most organs, TLRs act as a warning system that triggers an inflammatory response to threats. But in skin cells, the two identified HDAC enzymes, HDAC8 and HDAC9, inhibit the inflammatory response.

"This is one of the first demonstrations of how the microbiome can interact with epigenetic factors in the skin and modulate the skin's behavior through the inflammatory response," said George Sen, PhD, associate professor of dermatology and cellular and molecular medicine at UC San Diego School of Medicine. "Whatever environment we're facing can change a person's specific response to it. Since this epigenetic change is reversible, unlike alterations to our DNA, we can potentially control our skin inflammatory response through targeting of these enzymes."

The research was initially conducted in mouse models in which HDAC8 and HDAC9 had been genetically knocked out. As a result, the mice's skin could not tolerate microbial or viral exposures, resulting in a heightened immune reaction. The team then reproduced the findings with human cells in a culture dish.

Gallo said the work could change how doctors treat certain types of skin inflammation or other dermatologic conditions.

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