Despite the availability of various vaccines and antimicrobial drugs, viral and bacterial respiratory infections are responsible for high levels of morbidity and mortality worldwide. Ageing and co-morbidities (including chronic metabolic diseases) worsen the outcomes of respiratory infections. Our research group is focusing on two major respiratory pathogens: the influenza A virus and Pneumococcus. In 2020, we initiated a novel program on SARS-CoV-2, the aetiologic agent of COVID-19. Our general objectives are to
 (I) Define age- and comorbidity-associated factors that predispose to respiratory infections,
(II) Develop new strategies for reinforcing the host’s defence against respiratory pathogens.
Our group has a strong focus on the gut microbiota, which is known to be critical in human health and illness, and on adipose tissue, recently described to play a part during infection. We expect that a better understanding of the gut/lung/adipose tissue axis will be instrumental in conceiving novel treatment options for patients.

Our general objectives are to:
(I) define age- and comorbidity-associated factors that predispose to respiratory infections,
(II) develop new strategies for reinforcing the host’s defence against respiratory pathogens.
The group’s results have given it internationally acknowledged stature in this field. The group has recently patented several therapeutic applications in influenza and pneumococcal infections, including compounds produced by the gut microbiota such as short-chain fatty acids (SCFAs; grant: ANR ACROBAT). We have shown that these metabolites attenuate secondary disease outcomes during influenza - including bacterial superinfection (Cell Reports 2020). As during influenza, our recent data also show a functional alteration of the gut microbiota in preclinical models of COVID-19 (Gut Microbres 2021, 2022a, 2022b).Pharmacological approaches, prebiotics, and next-generation probiotics are being developed. These notably include bacterial strains selected for their strong anti-inflammatory potential and their ability to produce SCFAs in symbiosis with specific fibres.
Obesity, which corresponds to excessive white adipose tissue expansion, is one of the strongest reported risk factor for severe respiratory infections. We recently reported that influenza infection induces persistent alterations in whole-body glucose metabolism, and alters white adipose tissue’s inflammatory and metabolic functions, mostly characterized by the occurrence of brown-like adipocytes in the tissue (Commun Biol 2020, Cell Death Disease 2023). The mechanisms involved in white adipose tissue browning, in young adult and aged mice, are currently under investigation (CPER CTRL 19 FEDER DESTRESS-Flu).
We are characterizing the impact of ageing on respiratory infections. For instance, we are working on the influence of aging on the gut microbiota functionality in the context of respiratory infections (ANR  GUTSY). We also have a particular interest in the link between cellular senescence and respiratory infection (grants: ANR INFLUENZAGING and SENOCOVID). Our recent data indicate a deleterious role of naturally-occuring senescent cells during respiratory infections, inclusing COVID19 (Nature Aging 2023).  In collaboration with INSERM unit U1011, our data in elderly mice indicated links between the circadian oscillator, lung dysfunction, and altered antibacterial defences in the lung. We hypothesize that the uncontrolled expression of clock genes in aged lungs might impair innate immunity and thus result in defective antibacterial defences (CPER CTRL 19 FEDER and ANR DREAM).