Women are more likely to suffer from asthma compared to men due to the absence of testosterone, the male sex hormone. Testosterone avoids lungs from inhaling harmful pollen, dust and other airborne allergens by lungs claimed a study.
The study revealed that testosterone acts on immune cells as that are the key line of defenders of the body against foreign substances or invading viruses. These immune cells are directly linked to thesymptoms of asthma. The symptoms include inflammation and production of mucus in the lungs. These symptoms basically cause the airway to shrink during an asthma attack.
"Initially we thought that ovarian hormones would increase inflammation, more so than testosterone making it better," said Dawn Newcomb, from the Vanderbilt University in Tennessee, US.
"I was surprised to see that testosterone was more important in reducing inflammation," said Newcomb.
Previous studies have revealed that before puberty men are more likely to have a higher rate of asthma. Men have about 1.5 times higher rate more than women. However, after puberty women are double likely to suffer from asthma than men.
The researchers explained that once women hit menopause, asthma rates go down. These patterns contines till the menstruation ceases.
For the study published in the journal Cell Reports, the researchers paid attention to lung cells called Group 2 innate lymphoid cells or ILC2 cells. It made a certain protein named cytokines which cause inflammation and production of mucus in the lungs. This results in making the women difficult to breathe.
Through close examination, researchers discovered that blood from women suffering from asthma was found to have more ILC2 cells than non asthmatic women. The study concluded that asthmatic women were found to show relatively more ILC2 than men.
Additionally, when researchers added testosterone to the ILC2 cells, the male sex hormone prevented those cells from growing thus declining the production of protein- cytokines.
"However, sex hormones are not the only mechanism but, rather, one of many mechanisms that could be regulating airway inflammation," further added Newcomb.