Human Microbiota - Xenobiotics Interactions Lab
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Research
Our Projects
Trace elements and gut microbiota pathogen colonization resistance
We are interested in understanding on how metal imbalances in the gut impact the fitness and functioning of gut microbes, specifically their resistance to pathogen colonization. Studies have shown that imbalances in trace elements can reduce the diversity and richness of gut commensals, altering microbe-microbe interactions and potentially enabling pathogen or pathobiont growth. For example, Zn deficiency – a risk factor for childhood diarrhoea – has been linked with decreased overall richness and diversity of gut bacteria, creating an environment favorable for the colonization of pathogenic Escherichia coli strains.
We are currently investigating metal-dependent metabolic pathways, transporters and enzymes promoting or silencing pathogen growth within gut microbial communities in a metal-dependent manner by using ‘omics”, functional genetic approaches and mice infection models.
Trace elements’ impact on the gut microbiome resistome
Due to the antibacterial properties of metals and their increased use across multiple domains like agriculture, animal husbandry, aquaculture, medicines, surgical devices, electronics, and in hospital settings, many bacterial genomes isolated from various environments harbor resistance genes to metals. These genes are often co-localized with antibiotic resistance genes, sharing similar regulatory elements and causing cross-resistance to these drugs.
We are interested in investigating whether metal imbalances in the gut select for bacterial populations resistant to metal toxicity or starvation. Additionally, we seek to understand how these communities may contribute to the susceptibility and spread of antimicrobial resistance genes in the gut microbiota.
Gut microbiome – drug interactions
Recent research has provided the first systematic insights into direct interactions between the gut microbiome and drugs, revealing hundreds of previously unidentified effects, such as drugs that inhibit bacterial growth and bacteria transforming and accumulating them.
These findings laid the groundwork for us to establish the interdependences between drugs and bacteria that only emerge as bacteria transition from isolated to communal growth, and to establish a bottom-up approach that can be used to disentangle bacteria-drug from bacteria-bacteria interactions within a community.
Employing this bottom-up method, scalable from simpler (in vitro) to more complex (animal) models, we aim to investigate the microbiome-dependent effects on the mode of action of drugs.
