Le mercredi 22 octobre, Madame Marie-Laure DELHEZ, titulaire d'un Master en sciences biomédicales à finalité approfondie et d'un Certificat de formation à la recherche en sciences biomédicales et pharmaceutiques, présentera l'examen en vue de l'obtention du grade de Doctorat en sciences biomédicales et pharmaceutiques, sous la direction de Monsieur Didier CATALDO.

Cette épreuve consistera en la défense publique d'une thèse intitulée : "Impact of exposure to diesel particles on the development of lung cancer". 

Changement de local : la défense de thèse publique de Madame DELHEZ se déroulera à l’amphithéâtre 204, bâtiment B4, Amphithéâtres de l'Europe.

Le jury sera composé de :

Alain COLIGE (Président), Ingrid STRUMAN (Secrétaire), Didier CATALDO, Jean-Louis CORHAY, Sophie LUCAS (UCLouvain), Thomas MARICHAL, Carine MUNAUT, Muriel PICHAVANT (Pasteur Lille).

Résumé de la thèse

A comprehensive understanding of the mechanisms by which air pollutant exposure drives cancer progression remains incomplete. Particulate matter has been shown in both in vivo and in vitro studies to induce genotoxicity and mutagenesis through oxidative stress. However, its impact on the pulmonary immune microenvironment and its role in modulating anti-tumour immune responses remain poorly characterized. Here we propose that diesel exhaust particles (DEP), a major component of PM2.5, known to be associated with lung cancer risk, promote cancer by acting on immune cells that harbour tumour cells in the lung tissue. By using murine models of acute and chronic exposure to DEP, we identify the infiltration of a specific subset of polymorphonuclear neutrophils (PMNs) which express CD14. These cells exhibit increased NET formation and more immune suppression demonstrated by gene expression and functional data. Focusing on KrasLSLG12D P53FL/FL mice, a KRAS-driven lung adenocarcinoma model, we observed that chronic DEP exposure exacerbated tumour progression, as evidenced by increased tumour burden, elevated proliferation of Ki67-positive tumour cells, and an immunosuppressed T cell phenotype. These findings collectively support a tumour-promoting role for DEP air pollutant through the induction of PMN-MDSC-mediated immunosuppression and T cell exhaustion, highlighting the need for public health policy initiatives aimed at reducing air pollution and its associated disease burden.