Host–microbe co-evolution fosters mutually beneficial relationships that support healthy physiology, including tissue homeostasis and immune and metabolic balance. When the host tissue microenvironment is perturbed, this equilibrium can shift, reshaping microbial behaviour and host responses in ways that promote pathogenesis and disease. Mucosal barrier surfaces such as the respiratory tract, gastroesophageal region, and uterine cervix are particularly vulnerable because they are continuously exposed to environmental and microbial challenges and rely on tightly regulated regenerative programs.

Our group aims to understand how changes in tissue state and microenvironmental context influence host–microbe interactions during early disease trajectories, including progression toward carcinogenesis. We develop and apply clinically relevant 3D organoid and complementary in vivo models to study host–pathogen crosstalk, epithelial regeneration, and barrier defence in a controlled, mechanistic manner. Using state-of-the-art approaches, including advanced microscopy, single-cell profiling, and spatial analysis of transcripts and proteins, we resolve cellular diversity, tissue architecture, and intercellular communication that together shape susceptibility versus resilience.