Chronic airway diseases such as asthma and COPD are common chronic respiratory diseases of varying severity, which can be fatal. They are a source of disability and major health care costs. Patients' quality of life is largely affected but current treatments are mainly symptomatic.

Our group's ambition is to better characterize these diseases with a hypothesis based on the primordial role of the bronchial epithelium in these conditions. Indeed, the epithelium plays a key role through its position at the interface between the host and the environment, constituting the first line of defense against various external aggressions. It is clearly demonstrated that the bronchial epithelium is abnormal in patients and epithelial deprogramming/reprogramming would be a good way to interfere with the natural history of these pathologies made of exacerbations, acute episodes and decline in respiratory function (chronic aspect).

Through our studies, we aim to develop novel biomarkers and identify new therapeutic targets with the hope of interfering with the advent of these diseases. To do this, our projects are based on an original model of in vitro reconstitution of fully differentiated pseudostratified bronchial epithelium at the air-liquid interface obtained directly from patient samples and which maintains the initial characteristics.

Our current lines of research envisage:

• The prevention and resolution of bronchial inflammation orchestrated by the epithelium, particularly in the context of virus-induced exacerbations,
• Understanding the communication networks between the epithelium and inflammatory cells e.g. eosinophils, NK cells or platelets.
• The mechanistic apprehension and reprogramming of the diseased bronchial epithelium,
• Development of innovative treatments through translational research based on cohorts and national and international networks.

Previous publications

Keywords: asthma, COPD, bronchial epithelium, viral-induced exacerbation