Interpretation of the Role of Eosinophils in Diffuse Interstitial Pneumopathies

Diffuse interstitial lung diseases (ILDs) represent a group of rare, heterogeneous disorders of various etiologies, all sharing a common histopathological feature: fibrotic remodeling of the pulmonary parenchyma induced by a chronic inflammatory process. Although the prevalence of ILDs in France has recently been estimated at 19.4 per 100,000 inhabitants per year, they are frequently encountered in clinical practice due to their need for specialized hospital care. ILDs are associated with significant morbidity and a poor prognosis, despite the heavy burden of current therapeutic strategies. This highlights the urgent need to identify new therapeutic targets for these diseases.

Eosinophilic polymorphonuclear cell could represent one such target. As a source of pro-fibrotic mediators such as TGF-β, they may contribute to pulmonary fibrosis from a clinical standpoint. Our hypothesis is that a component of bronchial exacerbation in ILD patients may involve a type 2 immune response through the recruitment and activation of eosinophilic polymorphonuclear cell.

Given their role in pro-fibrotic signaling, our objective is to characterize type 2 immunity parameters-focusing in particular on eosinophilic polymorphonuclear cell-using a multi-source approach in a cohort of ILD patients. If type 2 immunity is significantly present in this population (referred to as ILD-eosinophilic polymorphonuclear cell), the investigators will investigate the role of eosinophilic polymorphonuclear cell in vitro using a co-culture model involving eosinophilic polymorphonuclear cell and respiratory epithelial cells (both bronchial and alveolar). Based on the results obtained, future prospects include evaluating the effects of biotherapy within this model as a preliminary step toward a subsequent clinical study.