JULIETTE DIREUR

With a background in pharmacy and a specialization in research, I discovered my interest in toxicology during my studies. This interest led me to enrol in the Master’s program "Human Toxicology, Risk Assessment, and Vigilance" at Université Paris-Saclay in my sixth year, where I was able to deepen my knowledge of the effects of toxic substances and the challenges related to public health. The EUR-LIVE scholarship allows me to pursue this path by conducting a PhD within the Lanone team at IMRB. My research project focuses on the impact of air pollution on the resolution of inflammation in cystic fibrosis, aiming to better understand the interactions between pollutants and respiratory pathophysiology. In the long run, I aspire to continue working in toxicology, combining research, prevention, and risk assessment for human health.

Research Project:

"This PhD project aims to test the hypothesis that air pollution could explain the variability in respiratory disease progression among cystic fibrosis (CF) patients by affecting the resolution phase of inflammation.

Some studies have begun to highlight the intrinsic mechanisms contributing to the chronic and ineffective airway inflammation characteristic of cystic fibrosis, particularly reporting abnormalities in synthesising specialized pro-resolving mediators (SPMs) involved in inflammation resolution. However, the cellular and molecular events underlying the abnormal synthesis of SPMs in cystic fibrosis are not fully understood and are not directly linked to microbial infections resulting from ion transport defects and impaired mucociliary clearance—both consequences of CFTR gene mutations in this disease. More broadly, the phenotypic variability of inflammatory lung disease in CF patients and their response to treatment suggest the involvement of factors beyond CFTR mutations.

Air pollution may play a role in this variability, as numerous epidemiological studies indicate that exposure to air pollution increases the vulnerability of patients with pre-existing chronic inflammatory diseases, including cystic fibrosis. Moreover, certain pollutants, such as ozone (O₃), titanium dioxide, diesel exhaust gases, and particulate matter (PM), have been shown to impact SPM biosynthesis. However, the potential role of air pollution in the dysregulation of SPM metabolism in cystic fibrosis, as well as the protective role of SPMs against pollution-induced airway damage, remains unexplored.

The aim of this project is to study the effects of urban pollution—using a realistic atmospheric simulation chamber—on primary respiratory epithelial cultures derived from cystic fibrosis patients."