A research group led by Associate Professor Minako Ito of Kyushu University has discovered for the first time in the world that stress hormones increased by asthma during pregnancy increase the risk of asthma in the child.
Environmental factors during pregnancy (such as smoking, stress, and maternal asthma) are known to increase the risk of developing asthma in offspring. Type 2 innate lymphoid cells (ILC2s) play an important role in allergic inflammation, including asthma. However, it has not been elucidated how asthma during pregnancy affects fetal immune cells and how it is related to the onset of asthma in offspring.
The research group investigated offspring born to mice with asthma and found that the number of ILC2 in the lungs increased and their function in inducing allergic responses also increased, leading to worsening asthma. It was revealed that maternal asthma maintains common epigenetic (a mechanism that regulates gene activity) changes in ILC2 in the fetal and adult lungs, resulting in excessive allergic responses to allergens. It was also found that exposure of the mother to the stress hormone glucocorticoid during pregnancy caused similar changes in fetal lung ILC2 as in the mother's asthma, exacerbating allergic inflammation in the offspring.
This clarified the importance of controlling maternal asthma and managing stress during pregnancy to reduce the risk of asthma in children. In addition, glucocorticoids are steroids, and the fact that steroid treatment can enhance ILC2 function and increase the risk of asthma is said to be a clinically important discovery. It is expected that this finding will contribute to understanding asthma treatment during pregnancy and its effects on the fetus, and to finding safe and effective management methods.