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Chronic respiratory diseases are a major cause of mortality and morbidity. The respiratory tree is located at the interface between environment and host, and as such plays a critical role in the development of the host immune response that can be either beneficial or deleterious. This immune response is one pathway to target, to modify the natural evolution of respiratory diseases.. Among them, the team studies two respiratory diseases, the acute respiratory distress syndrome (ARDS), often of infectious origin, and severe asthma.  Due to strong links with the pneumology and critical care departments of the CHU of Lille, we are very focused on translational research from the bench to the clinic.
In the context of ARDS, a link has been shown between low levels of endocan, a proteoglycan cloned in the lab, and the development of ARDS during septic shock (Gaudet et al, J Crit Care, 2018). This led us to evaluate endocan in a cohort of COVID patients hospitalized in critical care depertment of Foch Hospital (Suresnes). The results have shown that endocan was increased in COVID versus non COVID patients, and that patients developing the more severe ARDS had the lowest levels of endocan between D3 and D5 following tbeir admission in critical care,. These data suggest a predictive role of this molecule in in the development of ARDS in COVID patients (Pascreau et al, Crit care, 2021).
In the context of asthma, this disease remains a major challenge because of the diversity of its clinical phenotypes and biological mechanisms. Severe asthma concerns 5 to 10% of total asthmatics (more than 300 millions people in the world), but generates almost the totality of health costs devoted to this disease. Severe asthma is divided schematically in T2 asthma (with an eosinophilic profile) and non T2 asthma (with a neutrophilic or mixed profiles). These patients have frequent exacerbations that can be triggered by infections, allergen exposure or pollutants. In this context, the pulmonary immunity team decipher the immunobiological mechanisms involved in asthma, to propose novel therapeutic targets, by using original experimental models of asthma, and cohorts of asthma patients. We have in particular shown in a T2 experimental model of house dust mite (HDM) allergic asthma that sensing by NOD1 of some bacteria associated to HDM aggravates the severity of asthma in vivo, and that inhibiting this pathway may be a therapeutic approach for asthma (Ait Yahia et al, J Allergy Clin Immunol, 2021). In another model of non T2 asthma induced by dog allergen and inducing a strong bronchial remodelling, inhibition of the pathway leading to IL-22 production attenuates this phenotype (Bouté et al, Allergy, 2021). You will find at the bottom of the page two 3D videos showing bronchial remodelling visualizing collagen fibers (in green) by two-photons microscopy in the lung at baseline, and after allergen challenge in the non T2 model (collaboration E Weirkmeister, Team microbiologie cellulaire et physique de l'infection). As there is currently no biotherapy targeting non T2 asthma, these results are very promising, and studies of proof of concept are underway (START AIRR funded by region Hauts de France) modified mice as well as in asthma patients.

More information about the team : HERE

Peribronchial type I collagen fibers are visualized in green through the generation of second harmonic (SHG) signals by two-photon microscopy in the lung at baseline. The other lung structures appear in red.

Peribronchial type I collagen fibers are visualized in green through the generation of second harmonic (SHG) signals by two-photon microscopy in the lung after dog allergen challenge. Note the triple helical collagen molecules around bronchi.


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