Immune Detection and Elimination of Pathogens

Over the last 20 years, cell deaths emerged as crucial processes driving inflammation, host defense against infections and pathologies. To understand the determinants of various cell deaths, microbial interactions with cells are a fantastic field of investigation as pathogens use virulence factors to modify the regulation of various host-derived cell death pathways.

The group aims to expand and strengthen the knowledge already developed but also to tackle the challenges of tomorrow in the field of cell death, immunity, host pathogen interactions but also environmental exposure. Indeed, during infections, strongly influencing the vital prognostic of patients are the intrinsic microbial characteristics as well as environmental, age, sex and genetic parameters.

Inflammasomes are intracellular multi-protein complexes that play essential functions in immunity against pathogens. Specifically, inflammasomes both promote a regulated form of cell death termed pyroptosis and trigger the release of the key inflammatory cytokines interleukin (IL)-1β and IL-18, two important processes in controlling microbial infections. Because of their involvement in various pathophysiological conditions, our understanding of inflammasomes has generated an ever-growing interest in the scientific and medical communities over the last 20 years. Yet, most of this knowledge comes either from the use of rodent models, which may lack the specific structural and functional characteristics of human inflammasomes, or from the use of immune cells, which express a wide range of inflammasomes but lack inflammasomes specifically enriched in non-immune cells.

Thus, we study crucial and yet unexplored functions of unique human inflammasomes in epithelia (skin & corneal keratinocytes, airways, lung & intestinal epithelial cells) and in other compartments (e.gs neurons, endothelial cells). We further address inflammasome regulation and functions in atypical and yet understudied immune cells, namely the granulocytes neutrophils and eosinophils as well as in mast cells, critical sentinels of the immune responses.

To address these issues, we use a combination of technologies in microbiology, immunology, biochemistry, molecular and cell biology in various human cellular models developed in the group, including primary human epithelial organoids and organ on a chip.

This multidisciplinary research generates major discoveries in the regulation of human inflammasomes and their interactions with microbial pathogens and various environmental threats.

Contacts for interested students, post-docs, technicians/engineers, researchers, lecturers and others :
etienne.meunier@ipbs.fr
celine.cougoule@ipbs.fr

Team members

Research Scientists

Céline Cougoule (CNRS)
Raoul Mazars (University of Toulouse)
Etienne Meunier (CNRS)

Research Engineers

David Pericat (CNRS)
Chloé Rives

Postdoctoral Fellow

Thomas Benoist
Caio Bomfim

PhD Students

Léa Fromont
Andréa Gomes
Margaux Paradis
Léa Ravon-Katossky
Romain Vergé
Lylia Hakem

Embedded Emerging Research Team

Virginie Stévenin (Emerging PI – FRM)

Our research projects

To unlock the immune response: The cellular and molecular means by which intracellular sensors detect pathogens

To shortcut the intracellular PRRs: Non-canonical functions of cytosolic-derived sensors

Stromal immunity: To decipher the immune and microbicidal responses of the epithelia

Gorse et al. (2025) Portimine A toxin causes skin inflammation through ZAKα-dependent NLRP1 inflammasome activation.Cell Rep

Blot et al. (2024) Leishmania infantum exploits the anti-ferroptosis effects of Nrf2 to escape cell death in macrophages. Mol Cell

Rozario et al. (2024) Mechanistic basis for potassium efflux-driven activation of the human NLRP1 inflammasome. Proc Natl Acad Sci USA

Pinilla et al. (2023) EEF2-inactivating toxins engage the NLRP1 inflammasome and promote epithelial barrier disruption. J Exp Med

Leo-Icaza et al. (2023) Druggable redox pathways against Mycobacterium abscessus in cystic fibrosis patient-derived airway organoids. PLoS Pathog

Planès et al. (2022) Human NLRP1 is a sensor of pathogenic coronavirus 3CL proteases in lung epithelial cells. Mol Cell

Iakobachvili et al. (2022) Mycobacteria-host interactions in human bronchiolar airway organoids. Mol Microbiol.

Murine macrophage infected with Francisella novicida (Red) and stained for LC3 (Green).