[CEPCEB_All] IIGB Seminar: Audrey Le Gouellec *TOMORROW*

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*Audrey Le Gouellec*
*Univ. Grenoble Alpes, CHU Grenoble Alpes, CNRS, TIMC Lab, Grenoble, France*

Dr Audrey Le Gouellec is an associate professor and hospital practitioner
in the Department of Biochemistry at the School of Medicine, Université
Grenoble Alpes, CNRS, France. Her research focuses on host–pathogen
interactions, microbial adaptation, and the role of metabolism and
microbiota in infectious diseases. She heads the GEMELI mass spectrometry
metabolomics platform, serves as President of the French-speaking
Metabolomics and Fluxomics Network (Réseau Francophone de Métabolomique et
Fluxomique, RFMF), and is Deputy Director of the ED ISCE doctoral school.
Combining metabolomics with multi-omics and clinical data, she investigates
how pathogens adapt during chronic infections and how these mechanisms may
inform new therapeutic strategies.

*Towards a holistic approach to studying host–pathogen interactions and
medical applications*

*       Date:* Friday, March 6

*          Time:* 12:00 pm-1:00pm

*             Location: *Genomics Auditorium 1102


*Abstract:*
Host–pathogen interactions are increasingly understood as dynamic
ecosystems shaped not only by microbes and host responses, but also by
metabolism and the surrounding microbiota. In cystic fibrosis (CF), chronic
lung infection by Pseudomonas aeruginosa provides a powerful model to study
pathoadaptation over time. Using untargeted LC-HRMS/MS metabolomics
combined with clinical, phenotypic, genomic, and transcriptomic data, we
investigated longitudinal P. aeruginosa isolates from CF patients to
identify convergent metabolic adaptations associated with virulence. Our
results revealed three major metabotypes, with polyamines—particularly
spermidine—emerging as key discriminant metabolites linked to virulence
traits and to instability in lung function. Follow-up functional analyses
showed that spermidine biosynthesis is tightly regulated through
complementary pathways and directly contributes to cytotoxicity and
expression of virulence-associated mechanisms. Beyond bacterial adaptation,
our work also highlights the importance of considering the broader
microbiota and host metabolic context in CF exacerbations. Altogether,
these findings support a more holistic approach to host–pathogen
interactions, positioning polyamine metabolism as both a biomarker of
pathogenic adaptation and a promising therapeutic target to disarm rather
than kill pathogens.
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