Towards targeting the origin of the inflammatory cascade in asthma

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Promotion A. Gay

Aurore Gay’s thesis, we deepen our understanding of the mechanisms behind asthma. Asthma is a complex and common respiratory disease, for which no cure is yet available. By better understanding it, we get better chances to treat it.

The focus of this thesis is on the bronchial epithelial cells, the cells of the lung directly in contact with inhaled air. These cells protect the body against foreign particles, such as bacteria, viruses, or dust. In asthma, this defense mechanism is impaired. For non-asthmatics, some cells produce mucus to capture these microbes, and some cells with cilia push these microbes back out of the lungs. For people with asthma, there are fewer cells with cilia, and more mucus is produced, leading to mucus accumulation and difficult breathing. In addition, bronchial epithelial cells send signals that over-activate the immune system, which contributes to asthma symptoms.

This thesis investigates the differences in bronchial epithelial cells between asthmatics and non-asthmatics. This thesis describes in more detail than before the changes in composition and function of bronchial epithelial cells in patients with asthma, and how they change their behavior in response to a virus, or to signals from the immune system. We also show which differences are inherent to asthma, and which differences are a consequence of having asthma for a long time.

Finally, this thesis presents some approaches to help identify the patients with asthma who are likely to respond to current treatments, and to identify targets for novel asthma treatments.