With the summer heat, many Canadians no doubt will be replacing those long pants, shirts, and sweaters with shorts, tees, and swimwear. However, for up to one-sixth of our population, this choice may not come as easy as we think. It's because they suffer from a disease known officially as atopic dermatitis although most of us call it eczema.
Eczema is a difficult disease to pin down. The symptoms range from itchy rashes to cracked, oozing skin. This condition can be a mere annoyance but in severe cases, it can impact one's ability to function in society. The same difficulties can be said for treatment. Some can manage the condition with hygiene while others may require prescription medications.
When it comes to the cause, eczema has proven to be an enigma. Researchers have known for years the ailment arises due to a change in one's immunity. For some reason, the body tends to overreact in certain areas of the body leading to the symptoms. This explanation is the basis for numerous pharmacological treatments known to calm the immune response and reduce or eliminate the ailment.
While therapeutic options may be helpful for those suffering, for public health officials, there is a need to know why eczema happens. They need to understand how this alteration of immunity starts in the first place. If they can figure out why our defense forces go awry, they can develop steps to prevent the problem.
The most obvious potential culprits behind this disease are microbes. They can be found all over the skin and research has revealed different parts of the body have different microbial populations. One or more species could find themselves in areas where they don't belong, such as the elbows or the back of the knees, and in an infection-like process, force the immune system to alter in a manner that leads to symptoms.
This idea does seem sound and evidence has been shown to support this theory. Yet it has never been proven. The closest researchers have come is the identification of reduced microbial diversity in flare sites. However, no one has singled out one species.
Now that has changed thanks to a group of American researchers. They have devoted their attention to the microbes found in eczema. In the process, they have revealed the name of the most likely culprit. Unfortunately, the research also has led to even more questions.
The team collected microbial samples from children suffering from varying degrees of eczema. They also collected control samples from times when the kids were not suffering from flares. The hope was to find some distinct change in the types of microbes present and pinpoint one species as being the cause.
When these initial results came back, there was reason for hope. As seen in other studies, flares led to a reduce diversity of bacteria in the area. A closer examination revealed one particular species, Staphylococcus aureus, tended to be higher during symptoms. Moreover, more of this species meant worsening symptoms.
Right off the bat, this discovery makes perfect sense. The species is known to be involved in many skin conditions, including acne, impetigo, and rashes. But this result cannot explain why some individuals end up with eczema while others have no issues.
The answer comes in a subcategory of a species, known as strains. S. aureus has numerous different strains and each one acts differently from the rest. In this light, one or more strains might be responsible for causing the disease.
Not surprisingly, this is the direction the researchers went next. The team examined the diversity of the strains in the hopes of finding an appropriate culprit. As expected, they found blooms of single strains in the eczema areas. The path to an answer became a little clearer.
But the elation didn't last long. When the group compared these single strains among the different eczema patients, they found something rather unsettling. Each patient had a different troublesome strain.
This significantly increased the complexity of the situation and required the group to take the investigation to a new level. They needed to find out if these strains were producing a common molecule that led to symptoms.
The team explored the genetic information of the bacteria in the hopes of finding a common cause for the symptoms. They came across many potential candidate molecules yet none were expressed in all the strains. Rather than being able to hone in on a particular gene, the team realized the onset of symptoms was more complicated than they believed.
While the results of the study did not manage to find the smoking gun, the group did develop some useful information for public health officials. The onset of eczema is due to a lack of microbial diversity on the skin and S. aureus is the most likely candidate for trouble. Moreover, seeing blooms of a particular strain could spell trouble.
The discovery may lead to the development of new diagnostic measures to determine the risk for flares. This also may develop a new treatment concept in which the immune system is not targeted but the bacteria population. By increasing diversity through the addition of friendly microbes, eczema may be both prevented and treated.
If this direction pans out, the future of eczema prevention may come in a cream consisting of a diverse microbial population. All one would have to do is use it regularly when trouble arises. That way, they might be able to lose the worry about symptoms and confidently enjoy wearing those summer clothes.
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