- Asthma is a respiratory condition characterized by breathing difficulty
- Women are more likely to suffer from asthma than men. This may be due to the role of the male hormone called testosterone
- A new study found that testosterone protects men against developing asthma
The male hormone testosterone protects men against developing asthma, finds a study, explaining why women are twice more likely to develop asthma than men. Testosterone suppresses asthma triggers in men. This finding may lead to new targeted treatments for asthma.
Role of Testosterone in Preventing AsthmaA research by an international research team found that testosterone suppresses the production of a type of immune cell that triggers allergic asthma.
The study was conducted by Dr Cyril Seillet and Professor Gabrielle Belz from Melbourne's Walter and Eliza Hall Institute, with Dr Jean-Charles Guéry and his team at the Physiopathology Center of Toulouse-Purpan, France.
The research team hypothesized that hormones play a significant role in the incidence and severity of asthma in women. "There is a very interesting clinical observation that women are more affected and develop more severe asthma than men, and so we tried to understand why this was happening," Dr Seillet said.
The research team found that testosterone is a potent inhibitor of ILC2s. The ILC2s sensed testosterone and responded by halting the production of cells. Thus, men have low levels of ILC2s in the lungs, which is directly correlated with the reduced severity of asthma.
Professor Belz said, "Understanding the mechanism that drives the sex differences in allergic asthma could lead to new treatments for the disease."
Current treatment for asthma involves steroids, which are broad-based and can have significant side effects. The findings of the study could lead to new targeted treatments for asthma.
The findings offer a potential way of treating asthma by targeting the cells that contribute to the development of allergic asthma. The study also opens up the possibility of mimicking hormonal regulation of ILC2s as a way of treating or preventing asthma. "Similar tactics for targeting hormonal pathways have successfully been used for treating other diseases, such as breast cancer," said Professor Belz.
"Our research shows that high levels of testosterone in men protect them against the development of allergic asthma. We identified that testosterone is a potent inhibitor of innate lymphoid cells, a newly-described immune cell that has been associated with the initiation of asthma," said Dr Seillet.
The findings of the study are published in the Journal of Experimental Medicine.
AsthmaAsthma is a respiratory condition that narrows the airway, causing breathing difficulty. Asthma causes repeated episodes of wheezing, chest tightness and breathlessness. More than 334 million people across the world live with asthma. In the United States, about 18.7 million adults have asthma. One in nine Australians lives with this chronic lung condition. Some of the common triggers for allergic asthma include pollen, dust mites, cigarette smoke and pet hair.
Asthma in WomenIn adults, asthma is twice more prevalent in women than in men. Asthma could be severe in women and the ability to breathe can be affected by the menstrual cycle, pregnancy and menopause. Estrogen is a female hormone that can have an impact on the airways and trigger symptoms of asthma. The fluctuation of estrogen hormone may cause inflammation in the airways. Studies have shown that stabilizing estrogen levels can help control asthma attacks.
Another reason why women are more prone to asthma is that women have smaller lungs and narrower bronchial tubes than men. Understanding the gender differences is important in providing a personalized management plan for those who suffer from asthma.
- Sophie Laffont, Eve Blanquart, Magali Savignac, Claire Cénac, Gilles Laverny, Daniel Metzger, Jean- Philippe Girard, Gabrielle T. Belz, Lucette Pelletier, Cyril Seillet, Jean-Charles Guéry. Androgen signaling negatively controls group 2 innate lymphoid cells. The Journal of Experimental Medicine, (2017); jem.20161807 DOI: 10.1084/jem.20161807