New findings bring researchers one stop closer to better asthma treatment

New findings may help researchers better treat asthma symptoms.

Asthma is a chronic and sometimes lifelong condition that affects an individual's lungs. The disease can cause a number of symptoms, including tightness in the chest, shortness of breath, coughing and recurring periods of wheezing. Although most sufferers experience symptoms in early childhood, the condition can affect people of all ages. According to the National Institutes of Health, there are more than 25 million Americans who suffer from asthma – 7 million of whom are children.1

An overview of asthma
Someone who has been diagnosed with asthma will have inflamed airways, which makes it difficult for the lungs to function properly. There are often things that will trigger additional sensitivity to the area – such as the inhaling of certain substances. When the body is fighting an attack, it may cause the cells within the airways to create more mucus than usual, which makes it even more difficult for the person to breath normally.

Currently, there is no cure for asthma, but medical professionals have come a long way in managing the disease. This means that sufferers are able to maintain regular lifestyles that involve physical activity. However, even when symptoms are at ease, a flare can occur at any time. This is why those in the health care professional continue to research the condition.

New research findings
In early January 2013, professionals from the University of British Columbia continued research on the gene ORMDL3, which had recently been shown to have a link to early-onset asthma susceptibility.2 This was following previous research which showed that levels of this gene were found to be elevated among asthmatic patients. So, researchers aimed to ORMDL3 manipulation to reduce inflammatory responses. Unfortunately, their attempts were not successful.

However, when researchers from the University of Minnesota dove into a study surrounding the gene, they found useful information regarding the role ORMDL3 plays in asthma.3 What these investigators found was that the gene affects the body's ability to recruit inflammatory cells when an allergic reaction is taking place in the airways.

"While exciting, our finding is just one piece of the puzzle," Dr. Srirama Rao, one researcher of the study, said in a statement. "The more we understand about various asthma susceptibility genes including ORMDL3, the better positioned we will be to strategize new treatment options."

Details of the findings
Through their study, professionals from U of M were able to demonstrate the role in which the gene ORMDL3 plays regarding instances of allergic inflammation to the lungs.4 When there is too much of the gene present during the time of an asthma attack, the experienced symptoms worsen. The study showed that this was the result of ORMDL3's regulation of eosinophil – white blood cells that are responsible for helping the immune system fight off parasites – trafficking, recruitment and degranulation.

With this information, researchers are eager to conduct additional studies in hopes of finding better treatment options for asthma. However, more information is required for a better understanding of how this gene and others affect asthmatic patients.

Medex Supply provides asthma management supplies to both health care professionals and private parties. It is important that sufferers of the disease have the proper respiratory supplies for treating their condition at all times.

1 National Institutes of Health, "What is asthma?" June 15, 2012
2 Allergy, Asthma & Clinical Immunology, "Functional analysis of the impact of ORMDL3 expression on inflammation and activation of the unfolded protein response in human airway epithelial cells" February 1, 2013
3 University of Minnesota, "U of M research uncovers gene's contribution to asthma susceptibility" September 23, 2013
4 Nature Communications, "ORMDL3 promotes eosinophil trafficking and activation via regulation of integrins and CD48" September 23, 2013

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