Current research suggests that stress may activate immune cells in your skin, resulting in inflammatory skin disease. The related report by Joachim et al., “Stress-induced Neurogenic Inflammation in Murine Skin Skews Dendritic Cells towards Maturation and Migration: Key role of ICAM-1/LFA-1 interactions,” appears in the November issue of The American Journal of Pathology.Skin provides the first level of defense to infection, serving not only as a physical barrier, but also as a site for white blood cells to attack invading bacteria and viruses. The immune cells in skin can over-react, however, resulting in inflammatory skin diseases such as atopic dermatitis and psoriasis.

Stress can trigger an outbreak in patients suffering from inflammatory skin conditions. This cross talk between stress perception, which involves the brain, and the skin is mediated the through the “brain-skin connection”. Yet, little is know about the means by which stress aggravates skin diseases.

Researchers lead by Dr. Petra Arck of Charité, University of Medicine Berlin and McMaster University in Canada, hypothesized that stress could exacerbate skin disease by increasing the number of immune cells in the skin. To test this hypothesis, they exposed mice to sound stress. Dr. Arck’s group found that this stress challenge resulted in higher numbers of mature white blood cells in the skin. Furthermore, blocking the function of two proteins that attract immune cells to the skin, LFA-1 and ICAM-1, prevented the stress-induced increase in white blood cells in the skin.

Taken together, these data suggest that stress activates immune cells, which in turn are central in initiating and perpetuating skin diseases. Fostered by the present observation, the goal of future studies in Dr. Arck’s group is to prevent stress-triggered outbreaks of skin diseases by recognizing individuals at risk and identifying immune cells suitable to be targeted in therapeutic interventions.

The research, published in the October issue of the prestigious international journal Science, details how a huge molecule called a stressosome protects bacterial cells from external stress and danger.

Scientists from the University of Newcastle in Australia, and Newcastle University and Imperial College in the United Kingdom, collaborated on the discovery.

Associate Professor Peter Lewis from the Faculty of Science and Information Technology at the University of Newcastle in Australia said until now, researchers had not fully understood how bacteria responded to stress and potential danger.

“It is important to understand the changes that occur when bacteria are under stress as this is the point at which they are likely to become most infectious.

“The protein molecules that make up the stressosome are found in a very wide range of bacteria.  Some of these bacteria cause diseases such as listeriosis that has a 30 per cent mortality rate, and melioidosis that has a mortality rate as high as 90 per cent and is a significant health problem in northern Australia and south-east Asia.

“With bacteria becoming increasingly resistant to antibiotics, understanding how the stress response is controlled could lead to the development of drugs that help prevent bacterial infection from occurring.”

Lead author of the Science paper, Professor Rick Lewis from Newcastle University in the United Kingdom, said the team used groundbreaking techniques to observe the stressosomes.  Electron microscopy techniques were developed by Professor Marin van Heel of Imperial College and Associate Professor Peter Lewis developed the fluorescence microscopy imaging techniques.

“We knew that when bacteria were stressed, a warning signal would be sent from the surface to the inside of the cell.  The stressosome would then respond by triggering new proteins in the cell to react to the stress.

“Our latest work has revealed the structure and number of stressosomes per cell.  This has helped us understand how quickly the stressosomes respond to external stresses and prepare the cell to adapt to changes in its environment and ensure its survival.”

A bacteria cell’s ‘crisis command centre’ has been observed for the first time swinging into action to protect the cell from external stress and danger, according to new research out today (3 October) in Science.

The research team behind today’s study says that finding out exactly how bacteria respond and adapt to stresses and dangers is important because it will further their understanding of the basic survival mechanisms of some of the most resilient, hardy organisms on Earth.

The crisis command centre in certain bacteria cells is a large molecule, dubbed a ’stressosome’ by the scientists behind today’s research.  These cells have around 20 stressosomes floating around inside them, and although scientists knew they played an important role in the cell’s response to stressful situations, the complexities of this process had not been fully understood until now.

If a bacteria cell finds itself in a dangerous situation for example, if the temperature or saltiness of the bacteria’s environment reach dangerous levels which threaten the survival of the bacteria -a warning signal from the cell’s surface is transmitted into the cell.

Using cutting edge electron microscopy imaging techniques the authors of the new research observed that the stressosomes receive this warning signal, and in response several proteins called RSBT break away from the large stressosome.  This breakaway triggers a cascade of signals within the cell which results in over 150 proteins being produced proteins which enable the cell to adapt, react and survive in its new environment.

Professor Marin van Heel from Imperial College London’s Department of Life Sciences, one of the corresponding authors of the study, explains: “The cascade of events inside bacteria cells that occurs as a result of stressosomes receiving warning signals leads to particular genes inside the cell being transcribed more.  This means that some genes already active inside the cell are ‘turned up’ so that levels of particular proteins in the cell increase.  These changes to the protein make-up of the cell enable it to survive in a hostile or challenging environment.”

Dr Jon Marles-Wright from Newcastle University says: “Our work shows that cells respond to signals much like a dimmer on a light switch.  Now we’ll be building on this to work out how nature controls that dimmer switch.  We wouldn’t have been able to carry out this work without access to the Diamond synchrotron Light Source which has enabled us to examine the structures of individual stressosome proteins at atomic resolution.”

Dr Tim Grant, one of Imperial’s post doctoral researchers, adds that the key to bacteria cells’ success at surviving in rapidly changing environments is their speedy response: “The cell’s stressosomes are very good at their job as crisis command centres because they provide a very fast effective response to danger.  The chain reaction they kickstart produces results really quickly which enables bacteria to adapt to changes in their surroundings almost instantaneously.”

The team is now planning to collect very high resolution data of the stressosome complex on the world’s newest high-resolution cryo electron microscope, the FEI “KRIOS” that has just been installed in the Max Planck Institute in Martinsried, Germany.  Improving the resolution of the stressosome structure by a factor of two will lead to a resolution range normally only attainable by X-ray crystallography and will allow the researchers to directly see the amino-acid components of this fascinating complex.

In infancy, genes are the key influence on a child’s ability to deal with stress. But as early as 6 months of age, parenting plays an important role in changing the impact of genes that may put infants at risk for responding poorly to stress.That’s the message from a new study by researchers at the University of North Carolina-Chapel Hill, Pennsylvania State University, the University of North Carolina-Greensboro, and North Carolina State University. It appears in the September/October 2008 issue of the journal Child Development.

The researchers looked at 142 infants who had been placed in a stressful situation—being separated from their mothers—when they were 3, 6, and 12 months old. They measured infants’ heart rates while they were exposed to the stressor, isolating a cardiac response called vagal tone. Vagal tone acts like a brake on the heart when the body is in a calm state, but during a challenging situation, this brake is withdrawn, allowing heart rate to increase so the body can actively deal with the challenge.

They also collected DNA to determine which form of a dopamine receptor gene the infants carried; specific forms of this gene are related to problems in adolescence and adulthood including aggression, substance abuse, and other risky behaviors. To assess the mothers’ behavior as high or low in sensitivity, they also videotaped the mothers and their infants playing together for 10 minutes when the babies were 6 months old.

Both genes and parenting were found to be important to the infants’ development of the way in which the brain helps regulate cardiac responses to stress. At 3 and 6 months old, those infants with the form of the dopamine gene associated with later risky behaviors did not display an effective cardiac response to the stressor (a decrease in vagal tone which takes the brake off the heart so it can respond appropriately), while those infants with the non-risk version of the gene did. At these early ages, the researchers found, it didn’t appear to matter whether mothers were sensitive or not.

However, by the time the infants were 12 months old, the pattern changed. Infants with the risk form of the gene who also had mothers who were highly sensitive now showed the expected cardiac response while they were exposed to the stressful situation. Those infants with the risk form of the gene who had insensitive mothers continued to show the ineffective cardiac response to the stressor. These findings suggest that although genes play a role in the development of physiological responses to stress, environmental experience (such as mothers’ sensitive care-giving behavior) can have a strong influence, enough to change the effect that genes have on physiology very early in life. The researchers suggest this may be because of the cumulative effect on infants of exposure to their mothers’ behavior.

“Our findings provide further support for the notion that the development of complex behavioral and physiological responses is not the result of nature or nurture, but rather a combination of the two,” says Cathi Propper, research scientist at the University of North Carolina-Chapel Hill and the study’s lead author. “They also illustrate the importance of parenting not just for the development of children’s behavior, but for the underlying physiological mechanisms that support this behavior.

“Lastly, infancy is an important time for developing behavioral and biological processes. Although these processes will continue to change over time, parenting can have important positive effects even when children have inherited a genetic vulnerability to problematic behaviors.”

The increased beating of the heart that one experiences when in a stressful situation is just one part of the body’s response to stress, something often known as the “fight-or-flight response”. Another component of the fight-or-flight response is the suppression of pain, also known as stress-induced analgesia (SIA). Some of the nerves and nerve-produced peptides that are responsible for SIA have been identified, but much remains to be discovered. In a new study, a team of researchers in California, from AfaSci, Inc., Burlingame, and SRI International, Menlo Park, has revealed that nerves producing the peptide N/ORQ and nerves producing the peptide Hcrt are key in regulating SIA in mice.

The research team, which was led by Xinmin Xie and Thomas Kilduff, showed that in the brain of normal mice, Hcrt-producing nerve cells (Hcrt neurons) and N/ORQ-producing nerve cells interacted. N/ORQ affected the electrical current across Hcrt neurons and the release of neurotransmitters by these cells. Furthermore, administration of N/ORQ blocked SIA in normal mice, but this was overcome by administration of Hcrt at the same time. The authors therefore conclude that N/ORQ likely influences a variety of Hcrt-mediated processes, in addition to SIA, and suggest that these pathways might contribute to medical conditions caused by excessive stress, such as anxiety and post-traumatic stress disorder.