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Our previous highlighted teams

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.

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.

Our team studies the interactions between cells and tissues on the one hand, and bacteria, toxins, antimicrobial peptides and viruses on the other hand, by focusing on the mechanical and biological response. During the interaction, structural modifications are mechanically induced, which in turn will modulate a cellular or even tissue response.
The response we are studying is linked to the autophagy mechanism, which allows the cell to degrade microbes that enter the cells, but some of these microbes have developed, during the course of evolution, systems to escape or even exploit it.
Depending on the mechanical properties of the cells, structurally, the fluidity, elasticity and viscosity are modified. This concerns molecules, membranes and intracellular compartments. All of this helps to define the response capacity to the interaction between the micro-organism and the cell or tissue.
This is why we are developing a multidisciplinary approach combining biology and physics and designing innovative methods that enable us to remove conceptual barriers with regard to these interactions between host and microbes. If we can control these interactions or the responses they cause, then we can modulate their consequences.
We propose 4 short videos which, after a quick introduction on the general problem, describe subjects currently studied in the Group:
1- Mechanobiology from the molecule to the cell and tissue
2- Innovative technologies in host-pathogen interactions
3- Health benefits of lactic acid bacteria in the gut
4- Cellular responses to norovirus infections.

Have a good viewing!


Subjet #4

Subjet #3

Subjet #2

Subjet #1

Antibiotic (multi)drug resistance is a large and growing global health problem, particularly for tuberculosis and numerous nosocomial bacterial infections. In support of this, the World Health Organisation has proclaimed that research and drug development to combat these drug resistant bacteria is of critical priority. The CBA team investigates a series of novel strategies aimed to combat antibiotic resistant bacteria with current research focussing on the discovery and development of novel antibiotics and the development of innovate strategies that improve antibiotic penetration into bacteria.

To learn more about CBA team : HERE

The objectives of the team «Influenza, Immunity and metabolism» (I2M) are to better understand the physiopathological consequences of viral respiratory tract infections. We focus on influenza A virus and, more recently, on SARS-CoV-2, the aetiologic agent of COVID-19. We aim to study early immunological events developing in the lung tissue, and also outside the lungs. We integrate the impact of ageing and co-morbidities (dyslipidemia) in the host response to infection. This research recently led us to identify the gut-lung axis, and particularly the gut microbiota, as an important player of the host response. The adipose tissue is also sollicitated during infection and we try to disentangle the consequences on disease outcomes.  For this, we develop experimental models in link with clinicians. We expect that a better understanding of the gut/lung/adipose tissue axis will be instrumental in conceiving novel treatment options for patients.

To learn more about the team: HERE


One of our major focus concern the 3rd cause of death in the world: COPD.
You wish to discover more about it, and therapeutic application? Follow our series of 3 episodes.

Episode 3

Episode 2

Episode 1