Can Asthma-Causing Cells Be Reprogrammed?: A HealthCentral Explainer
New research shows that specific immune cells can be rewired so that they no longer cause inflammation in the lungs, which would be especially helpful for people with allergic asthma.
What is the study?
The study focused on specific immune cells, called T-helper 2 or TH2 cells, responsible for causing inflammation in the lungs. After identifying the enzyme Suv39h1, which modifies the DNA of the TH2 cells, researchers sought to reprogram the TH2 cells in mice.
The team of researchers, from the Institut Curie, National Centre for Scientific Research, National Institute of Health and Medical Research and Montpellier Cancer Research Institute, conducted the study in Paris, and published their results in the journal Nature.
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What did they find?
Using mice with allergic asthma, researchers used agents to inhibit the enzyme Suv39h1, which otherwise would “tag” the DNA of the immune cells to switch on certain genes for an allergic response. Researchers successfully blocked the pathway and reduced the airway damage in the mice caused by the allergic response.
What does it mean?
People with asthma have too many TH2 cells, which send signals that cause inflammation and damage in the upper airways. By identifying the enzyme responsible for turning on this gene in the TH2 cells, researchers have discovered a potential therapy which would target those enzymes and prohibit them from causing an allergic response.
According to James Thompson, M.D., HealthCentral’s asthma, allergy and cold & flu health pro, this research looks very promising. However, he says, there are a few other things to consider:
“Asthma genes have been the focus of genetic research for years. There are several gene sequences that have been associated with allergic hypersensitivity and asthma,” he says, however, targeting these genes may not be effective in the majority of asthma sufferers.
Furthermore, some people with asthma are not allergic, he says. “In fact, there are many different phenotypic expressions of asthma (meaning traits and characteristics of gene expressions that result from gene-environment processes or development). Some people just cough, others wheeze with almost every attack, others may primarily have shortness of breath, with no wheezing or coughing.”
In addition, he says further research would depend on whether the Suv39h1 gene exists in humans. The potential to help people with asthma is there, he says, because this gene is directly linked to causing inflammation, and all asthma patients have problematic inflammation in the lungs.
“This would be a major breakthrough in asthma research if an equivalent gene could be located and inhibited. I'm certain scientists are gearing up for the task since the human genome has already been fully mapped. It would not take long to locate this gene if the sequence of nucleotides is conserved over different species, but therein lies the challenge.”
Dr. Thompson does think this research could open the door to new ways to treat asthma.
“At some point in the future there may be a way to inhibit a similar gene in humans by some form of injection therapy. Perhaps even an inhalant--which would focus the medicine where you need it-- could be developed that would represent a new class of asthma medications. Of course, we are years of research and drug trials away from this, but the thoughts are not far-fetched based on capabilities in pharmacology achieved over the past few decades.”
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What about other allergies?
A study from January 2010 focused on how TH2 cells were created to see if there was a way to inhibit their ability to produce an allergic response altogether, and that could prevent allergic diseases, such as asthma, atopic dermatitis and food allergy.
Researchers from the University of Texas looked at dendritic cells, which initiate the immune response. These cells come into contact with other immune cells, T cells, which cause them to develop into either helper 1 (TH1) or TH2 cells. Both are important to the protective immune response, but as noted above, the TH2 cells are capable of driving an allergic response, which is an overreaction of the immune system. Previously it was not known how dendritic cells caused T cells to become TH2 cells.
Using the blood of healthy donors, researchers found that the binding of a certain protein called thymic stromal lymphopoietin (TSLP) activates a specific pathway within the dendritic cells, which then send messenger molecules to the T cells, causing them develop into TH2 cells.
Researchers say the TSLP acts as a switch that causes the development of the allergic response, which suggests that targeting the TSLP molecule could lead to treatment and prevention methods for allergic diseases.
Walter and Eliza Hall Institute. (2012, July 6). "Asthma-Promoting Immune Cells Can Be Rewired So They No Longer Cause Inflammation." Medical News Today. Retrieved from http://www.medicalnewstoday.com/releases/247480.php.
Walter and Eliza Hall Institute (2012, July 5). Rewiring DNA circuitry could help treat asthma. ScienceDaily. Retrieved July 12, 2012, from http://www.sciencedaily.com/releases/2012/07/120705133916.htm
NIH/National Institute of Allergy and Infectious Diseases (2010, January 20). Switch turns on allergic disease in people. ScienceDaily. Retrieved July 12, 2012, from http://www.sciencedaily.com/releases/2010/01/100120144003.htm