Host and microbe's co-evolution fosters a mutually beneficial relationship in maintaining healthy physiological processes, including tissue homeostasis, metabolic and immune function. Perturbations of the host tissue microenvironment affect this balance, promote microbial evolution and pathogenesis. The mucosal surfaces like the respiratory tract, gastro-esophagus, and uterine cervix are particularly prone to metaplastic and cancer development. Metaplasia, a precancerous condition, is an adaptive behavior of the tissue to withstand better the changing local environment of the tissue associated with external factors such as diet, acidic environment, or smoking.  However, it remains unclear why metaplastic sites of a given organ show enhanced susceptibility to microbiota alteration, infections, and transformation events. My group aims to understand the co-evolution of the host tissue microenvironment and pathogens during metaplasia and cancer development. We develop and apply 3D-organoid and in-vivo models to study host-pathogen cross-talks, tissue homeostasis, and model disease development. We adopt state-of-the-art technologies, including advanced microscopy, single-cell omics, and spatial analysis of transcripts and proteins to decipher cell types, spatial organization, and molecular cross-talks involved in pathogenesis.

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