Aberdeen Scientists Find Link Between Light Deficiency and Multiple Sclerosis

Aberdeen scientists have found that artificial sunlight can have a “striking effect” in helping treat sufferers of diseases such as multiple sclerosis.

Researchers from Aberdeen University studied patients in the north of Scotland – which has the highest rate of MS in the UK - who were being treated during winter with artificial UV (ultraviolet)-B light therapy for skin diseases caused by their immune systems acting inappropriately.

The research - published in the Journal of Allergy and Clinical Immunology – shows how UV-B light boosts vitamin D, as well as cells in our body that are responsible for regulating or balancing the immune system. Vitamin D is made in our bodies by UV-B light from the sun.

Some studies have suggested a link between vitamin D deficiency and autoimmune diseases such as MS.

This possible link might also explain the increasing prevalence of autoimmune disease among those living far from the equator, where there are lower levels of winter sun.

Autoimmune diseases - like MS and type 1 diabetes - are diseases where the immune system mistakenly attacks the body’s own tissues or harmless substances that enter the body.

Dr Anthony Ormerod, clinical reader in dermatology at the university, said: “Our study shows that UV-B light, which mimics sunshine, can have a striking effect on the immune system of patients.

“We found that UV-B light boosted the production of vitamin D, and of regulatory T cells, which play an important role keeping our immune systems in check.

“Our findings have important implications for future interventions including the recommendations for healthy lifestyle and a possible role for phototherapy and/or vitamin D supplementation in the prevention or treatment of autoimmune and inflammatory diseases.

“While too much exposure to sunlight is harmful and increases skin cancer risk, these results suggest that subjects in our study would have some benefits from small amounts equivalent to summer exposure in the winter but more work needs to determine the role of sunlight and the role of supplementing the diet with vitamin D.”

Dr Helen Macdonald, senior lecturer in nutrition and translational musculoskeletal research at the university and chair of the National Osteoporosis Society Nutrition and Lifestyle forum, said: “There are risks associated with high levels of both therapies, so it is important that we get the balance right.

“We would also want to stress that we are not advocating sun bed use since this is not the same type of radiation produced by sun beds which already have well-documented health risks.

“The average dose of UV light that the volunteers received was the equivalent to sunlight exposure in Aberdeen over spring and summer and further work is required to determine if lower doses are effective.”

Professor Mark Vickers, chair in applied medicine at the university, added: “Ours is the first study to demonstrate in patients a cause and effect between UV light, vitamin D and systemic immune function in people.”

Malaria evades the Human Body's Immune system

It’s known that malaria causes a highly inflammatory response in infected individuals that leads to the deadly clinical complications of anemia and cerebral disease.

The Yale research team learned that the parasites produce their own version of a human cytokine, or immune hormone, which directs the inflammatory response during malaria.

They also discovered that this cytokine, called PMIF, incapacitates the anti-malaria, memory T-cell immune response.

Using a genetically modified strain of the malaria parasite in mice, the Yale team found that PMIF causes host T-cells to develop into short-lived effector cells rather than protective memory cells.

The short-lived cells die during the infection, and the long-lived memory T-cells are not produced in adequate numbers to combat the infection or to protect from re-infection, which occurs repeatedly in malaria-endemic regions.

“These findings indicate that malaria parasites actively interfere with the development of immunological memory, and may account for the inhibition of protective immune responses in human malaria,” said Rick Bucala, M.D., professor of internal medicine, pathology, and epidemiology and public health at Yale School of Medicine.

• “This knowledge will help us identify specific therapies that can protect anti-malarial T-cells from death and improve an individual’s immune response to infection or to vaccination.”

More information: PNAS paper: www.pnas.org/conte… ull.pdf+html

Why a mother's immune system doesn’t reject the fetus

Researchers at NYU School of Medicine have made an important discovery that partially answers the long-standing question of why a mother’s immune system does not reject a developing fetus as foreign tissue.

“Our manuscript addresses a fundamental question in the fields of transplantation immunology and reproductive biology, namely, how do the fetus and placenta, which express antigens that are disparate from the mother, avoid being rejected by the maternal immune system during pregnancy?” explained lead investigator Adrian Erlebacher, MD, PhD, associate professor of pathology and a member of the NYU Cancer Institute at NYU Langone Medical Center. “What we found was completely unexpected at every level.”

The researchers discovered that embryo implantation sets off a process that ultimately turns off a key pathway required for the immune system to attack foreign bodies. As a result, immune cells are never recruited to the site of implantation and therefore cannot harm the developing fetus.

The study, funded by grants from the National Institutes of Health and the American Cancer Society, appears in the June 8 issue of Science.

A central feature of the body’s natural immune defense against transplanted foreign tissues and pathogens is the production of chemokines as a result of the local inflammatory response.

The chemokines recruit various kinds of immune cells, including activated T cells, which accumulate and attack the tissue or pathogen. The chemokine-mediated recruitment of activated T cells to sites of inflammation is an integral part of the immune response.

During pregnancy however, the foreign antigens of the developing fetus and the placenta come into direct contact with cells of the maternal immune system, but fail to evoke the typical tissue rejection response seen with organ transplants.

Several years ago, Erlebacher and his research team found that T cells, poised to attack the fetus as a foreign body, were somehow unable to perform their intended role.

The finding prompted the researchers to wonder if perhaps there was some sort of barrier preventing the T cells from reaching the fetus.

They turned their attention to studying the properties of the decidua, the specialized structure that encases the fetus and placenta, and there, in a mouse model, they found new answers.

The research team has discovered that the onset of pregnancy causes the genes that are responsible for recruiting immune cells to sites of inflammation to be turned off within the decidua. As a result of these changes, T cells are not able to accumulate inside the decidua and therefore do not attack the fetus and placenta.

Specifically, they revealed that the implantation of an embryo changes the packaging of certain chemokine genes in the nuclei of the developing decidua’s stromal cells.

The change in the DNA packaging permanently deactivates, or “silences,” the chemokine genes.

Consequently, the chemokines are not expressed and T cells are not recruited to the site of embryo implantation.

Also of note, the observed change in the DNA packaging was a so-called ‘epigenetic’ modification, meaning a modification that changes gene expression without the presence of a hereditable gene mutation.

“These findings give insight into mechanisms of fetal-maternal immune tolerance, as well as reveal the epigenetic modification of chemokine genes within tissue stromal cells as a modality for limiting the trafficking of activated T cells,” Dr. Erlebacher said.

“It turns out that the cells that typically secrete the chemoattractants to bring the T cells to sites of inflammation are inhibited from doing so in the context of the pregnant uterus. The decidua appears instead as a zone of relative immunological inactivity.”

Inappropriate regulation of this process, Dr. Erlebacher explained, could cause inflammation and the accumulation of immune cells at the maternal-fetal interface, which could lead to complications of human pregnancy, including preterm labor, spontaneous abortion and preeclampsia.

Erlebacher and his team will next look to see if these epigenetic modifications are also present within the human decidua, and whether the failure to generate them appropriately is associated with complications of human pregnancy.

He explained that the study’s findings also raise the possibility that the same kind of mechanism could enhance a tumor’s ability to survive inside its host. The findings could have implications for autoimmune diseases, organ transplantation and cancer, as well as pregnancy.

“This is a very exciting finding for us because it gives a satisfying explanation for why the fetus isn’t rejected during pregnancy, which is a fundamental question for the medical community with clear implications for human pregnancy,” Dr. Erlebacher said.

“It also reveals a new modality for controlling T cell trafficking in peripheral tissues that could provide insight into a myriad of other conditions and diseases.”

Early Detection of Immune Changes Prevents Painful Shingles in Astronauts

VZV infected MeWo cells showing typical herpes-virus-induced multinucleated giant cells. 

Cultures are stained with acrydine orange to identify RNA (red) in the cytoplasm. (NASA).

The physiological, emotional and psychological stress associated with spaceflight can result in decreased immunity that reactivates the virus that causes shingles, a disease punctuated by painful skin lesions.

NASA has developed a technology that can detect immune changes early enough to begin treatment before painful lesions appear in astronauts and people here on Earth.

This early detection and treatment will reduce the duration of the disease and the incidence of long-term consequences.

Spaceflight alters some elements of the human immune system: innate immunity, an early line of defense against infectious agents, and specific components of cellular immunity are decreased in astronauts.

Astronauts do not experience increased incidence or severity of infectious disease during short-duration spaceflight, but NASA scientists are concerned about how the immune system will function over the long stays in space that may be required for exploration missions.

Selecting one or more biomarkers or indicators of immunity in healthy individuals is difficult, but the herpes viruses have become valuable tools in early detection of changes in the immune system, based largely on the astronaut studies.

Eight herpes viruses may reside in the human body, and virtually all of us are infected by one or more of these viruses.

Herpes viruses cause diseases including common "fever blisters" (herpes simplex virus or HSV), infectious mononucleosis (Epstein-Barr virus or EBV) and chicken pox and shingles (varicella zoster virus or VZV).

In immune-suppressed individuals, herpes viruses may cause several types of cancer, such as carcinoma, lymphoproliferative disease and others.

According to the Centers for Disease Control and Prevention, one million cases of shingles occur yearly in the U.S., and 100,000 to 200,000 of these cases develop into a particularly painful and sometimes debilitating condition known as post-herpetic neuralgia, which can last for months or years.

The other seven herpes viruses also exist in an inactive state in different body tissues much like VZV, and similarly they may also reactivate and cause disease during periods of decreased immunity.

The most common cause of decreasing immunity is age, but chronic stress also results in decreased immunity and increases risk of the secondary disease, such as VZV-driven shingles.

Chemotherapy, organ transplants and infectious diseases, such as human immunodeficiency virus or HIV, also result in decreased immunity.

Thus, viral reactivation has been identified as an important indicator of clinically relevant immune changes.

Studies of immune-compromised individuals indicate that these patients shed EBV in saliva at rates 90-fold higher than found in healthy individuals.

The herpes viruses are already present in astronauts, as they are in at least 95 percent of the general adult population worldwide.

So measuring the appearance of herpes viruses in astronaut body fluids serves as a much-needed immune biomarker.

It is widely believed that various stressors associated with spaceflight are responsible for the observed decreased immunity.

Toxoplasma Gondii: How your cat could be making you ‘crazy’

It’s long been known that a microbe found in cat's can harm people with weakened immune systems, such as people with AIDS.

It’s also been known that pregnant women should avoid cat litter so they don’t catch the microbe, lest they pass it on to their babies, causing brain damage in the infants or even death.

The microbe in question is Toxoplasma gondii (T. gondii or Toxo for short).

New research from an unconventional scientist is showing that in certain circumstances, the microbe can alter our basic personalities, making us more or less outgoing, trusting and fearful, and even making us more prone to schizophrenia, car crashes and suicides.

The circumstances that create this possibility are as follows;

• We have to be infected by the microbe
• Our bodies will eventually overcome it, 
• But the parasite can lay dormant,
• and the danger lies in whether it lodges or travels to our brain cells

The researcher, the Czech evolutionary biologist Jaroslav Flegr, claims that when you consider all its impacts, “Toxoplasma might even kill as many people as malaria, or at least a million people a year.”

Read more of this article here: How your cat could be making you ‘crazy’

JC Polyomavirus: Deadly but with a weakness for sugar

It doesn’t strike often but when the JC polyomavirus does, it’s ruthless. The virus preys on people with weakened immune systems and almost always kills them.
Now the killer may have a target on its back. An international team has uncovered that the virus must bind to a very specific sugar molecule dangling from the side of the brain cells it attacks.

The finding, reported this week in the journal Cell Host & Microbe, could provide a basis for developing drugs to interrupt that process.

Researchers from Brown University, the University of Tübingen in Germany, and Imperial College in London painstakingly characterized the precise structure and biology of how the virus binds to host cells down to the atomic level.

By exposing a specific target, the work sets the table for drug development to begin, says Walter Atwood, professor of molecular biology, cell biology, and biochemistry at Brown and a senior author of the study.

“The overall goal is to get these ‘plans’ and then design small molecules—drugs that will fit in this receptor, binding and preventing infection,” Atwood says.

Atwood notes that this paper also marks the first time anyone has fully determined the structure and binding functionality of a human polyomavirus. While the JC polyomavirus causes the brain-wasting disease known as PML, others in the “family” are implicated in ailments such as skin cancers.

When the virus floats toward a cell, it encounters a metaphorical cityscape of sugary molecules on its surface, says Brown postdoctoral researcher Melissa Maginnis, one of the paper’s two lead authors. The team wanted to know which one the virus chooses.

Psoriasis: debilitating socially and emotionally

“Psoriasis is a predisposition for your immune system to react with your skin,” said Dr. Ellen Marmur, chief of the Division of Dermatologic and Cosmetic Surgery at Mount Sinai Hospital in New York City.

“Something that would normally… trigger a slight reaction in most of us, will trigger a domino effect in somebody with psoriasis.”

Beneath the surface, a psoriasis patient’s immune system overreacts and begins to attack itself. This abnormal activity is more characteristic of an autoimmune disease such as multiple sclerosis or rheumatoid arthritis.

Healthy skin regenertaes itself every 28 days but with psoriasis and as a result of inflammation, skin cells regenerate every two to four days, causing an excessive build up of cells.

When this happens, patches of the skin develop plaque, which is thick, red and scaly. The dead cells surface on top of irritated areas as loose, dry skin. They have a silver-white color and can flake off or crack. Depending on the type and severity, psoriasis can be painful and itchy.

In addition to the symptoms experienced, psoriasis patients who scratch their skin are likely to encounter or create further damage.

“If you scratch your skin, or if you have a piece of clothing that rubs against your skin in the area that is irritated, you can develop psoriasis. This is called the Koebner phenomenon,” said Dr. Mark Lebwohl, chairman of the Department of Dermatology at Mount Sinai School of Medicine and Mount Sinai Hospital.

Causes
Outbreaks are usually triggered by environmental factors like skin injuries; cold weather, infections, such as strep throat; bad reactions to medications; and even stress.

Psoriasis isn’t contagious. It can affect anyone and can plague anyone from babies to the elderly, Lebwohl said.

While some cases are so mild the patient doesn’t realise they have psoriasis, severe cases can be very debilitating and cover nearly the entire surface of the body.

The elbows, knees and scalp are the most common areas to be affected, however, psoriasis can present anywhere on the body, Marmur said.

Mild psoriasis is defined as 3 percent body coverage and severe psoriasis as 10 percent or more. Approximately 25 percent of those with psoriasis have a moderate or severe case.

There are a number of Types of Psoriasis
Where it turns up and how severe it is, has a lot to do with which of the five types of psoriasis you have.

1. Psoriasis vulgaris, also known as plaque psoriasis, is the most common, affecting more than 80 percent of all psoriasis patients. It can be a really well circumscribed pink, red plaque with a silvery or gray scale.

2. Guttate psoriasis is also red and scaly but smaller and typically covers larger body parts. It affects approximately 10 percent of psoriasis patients and can be triggered by strep throat.

3. Inverse psoriasis is red but doesn’t have the silvery-white scales. It presents as moist and red and covers smooth, creased areas of the skin like the armpits, the groin and underneath the breasts. Obese patients are most prone and tend to have more severe symptoms

A large portion of psoriasis patients are obese or become obese, said Lebwohl, who includes a heart-healthy diet as one course of action to improve your condition.

4. Pustular psoriasis looks like little spots of acne all over the body, Marmur said.

5. Erythrodermic psoriasis is the most severe form of the disease when plaque covers most of the body surface

Pustular and erythrodermic psoriasis are the rarest and the most dangerous. While they can occur independently, patients who develop them generally have plaque psoriasis. They are potentially fatal because they compromise the body’s ability to ward off infections and control body temperature.

“The typical story will be a patient with plaque psoriasis is given systemic steroids, cortisone,” Lebwohl said. “That clears psoriasis, but as you take them off of the steroids, you can develop a horrific flare where your body gets covered head to toe with red skin, or covered with puss pimples… Many of these patients will grow bacteria in their blood and can actually die from sepsis.”

Problems Associated With Psoriasis
Patients can become anemic from dangerously low amounts of protein in the blood, or suffer from other factors as a result of these debilitating forms of the disease.

When treating a psoriasis patient, doctors will ask a series of questions called the SF-36 to measure how it has impacted there lives.

In addition to its debilitating physical and psychological effects, psoriasis can force patients to miss work in order to manage their disease. Some of Lebwohl’s psoriasis patients have lost, or quit their jobs because of the amount of time they had to take off, he said. Others quit because of the embarrassment of not being able to perform.

“The National Psoriasis Foundation has looked at the incomes of patients and, basically, you can correlate income negatively with the various severities of the disease. The more severe, you’re going to earn less money,” said Lebwohl, who is also the chairman of the Medical Board of the National Psoriasis Foundation.

The disease is also linked to cardiovascular disease, diabetes and depression.

“Not only can it be debilitating socially and emotionally, but people with psoriasis also have a risk of other internal diseases,” Marmur said. “It’s like running your car at maximum, you’re just going to burn out other parts of the engine and infrastructure, other things are likely to premature wear or to be damaged.”

Dealing with the effects
Make sure you have been correctly diagnosed. Consult regularly with your doctor to ensure that you are receiving the best medical treatment. In addition to this, seek out local self help groups where you can share experiences and get practical advice. Keep up to date on the latest research but don't be the first one to try it.

Check what you are eating and try to establish living and healthy eating patterns, reducing your intake of artificial chemicals, sugar and caffeine. Also actively pursue activities which you enjoy and which relax you, give you a sense of well being. Learn to relax yourself through yoga, meditation or simply reading a book in a warm quiet room.

It is often difficult to mix well in groups and crowds because of the skin irritation but mainly because of the 'stigma' that makes you feel less worthy. Psoriasis and many other skin complaints do severely damage the self esteem and this leads to self isolation and exclusion from society. Seek out a good friend and ask for their help and support in keeping you socially active, simply by accompanying you to venues. To tell you the truth, we all do it, why not you?

National Psoriasis Foundation - Addressing Psoriasis

National Psoriasis Foundation - Addressing Psoriasis

August is Psoriasis Awareness Month

Each August, the National Psoriasis Foundation of the US, sponsors Psoriasis Awareness Month, dedicated to raising awareness, educating the public and dispelling myths about psoriasis.

Psoriasis is the most prevalent autoimmune disease in the U.S., affecting as many as 7.5 million Americans. It occurs when the immune system sends out faulty signals resulting in red, scaly patches on the skin that bleed and itch. Psoriasis is not contagious.

Psoriasis frequently occurs with a range of other health concerns including Crohn's disease, diabetes, hypertension, heart attack, depression and liver disease.

Up to 30 percent of people with psoriasis also develop psoriatic arthritis, which causes pain, swelling and stiffness around the joints. People with mild psoriasis are just as likely to develop psoriatic arthritis as those with moderate or severe forms of the disease.

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