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.”