Erinna Lee group
Gut Biology and Disease Signalling
Our lab investigates how cell death and survival pathways maintain intestinal homeostasis, and how their disruption drives gastrointestinal disease and broader systemic dysfunction. We focus on mechanisms such as autophagy, apoptosis, endocytic trafficking, and epithelial stress responses, which are essential for preserving gut barrier integrity, microbial balance, and tissue resilience. Using advanced 3D organoid models, genetic mouse systems, molecular and cellular biology, and multi-omics approaches, we aim to define how defects in these pathways initiate epithelial dysfunction, maladaptive inflammation, and disease. This work underpins our efforts to identify root-cause therapeutic targets for chronic intestinal disorders such as inflammatory bowel disease, where current therapies often suppress inflammation without correcting the underlying epithelial pathology.
A major extension of this program is understanding how gut dysfunction shapes systemic health, particularly its impact on brain ageing, cognition, and neuroinflammation. We investigate how intestinal barrier disruption and epithelial stress generate gut-derived immune, metabolic, and neural signals that influence the brain, with a focus on ageing, menopause-associated vulnerability, and neurodegenerative risk. This work aims to uncover whether targeting the gut can provide new strategies to preserve cognitive health and reduce neuroinflammatory decline. In parallel, we are also interested in how dysregulated cell death and survival pathways contribute to gastrointestinal cancers, including colorectal and pancreatic cancer, where these same pathways may influence tumour progression and treatment response.
Research areas
We explore how epithelial signalling pathways, including autophagy, apoptosis, and endocytic trafficking, govern gut integrity, barrier repair, and communication with the immune system. Our work has uncovered unexpected roles for key autophagy regulators in intestinal health, revealing how defects in these pathways initiate epithelial dysfunction giving rise to inflammation.
Most current inflammatory bowel disease (IBD) therapies suppress inflammation rather than correcting the underlying molecular defects that trigger disease. Our program seeks to define the molecular origins of gut epithelial stress and identify actionable therapeutic nodes that prevent inflammation from arising in the first place.
Chronic intestinal inflammation sends powerful metabolic, immune and neural signals throughout the body. We aim to uncover how these gut-derived signals influence the brain, with a focus on cognitive decline, neuroinflammation, and susceptibility to neurodegenerative diseases. These studies bridge gastrointestinal biology with neuroscience and lay the groundwork for targeting the gut as a modifiable upstream driver of brain health. This includes evaluating gut-focused interventions, such as GLP-1 receptor agonists and dietary strategies, to determine whether modulating epithelial function and barrier integrity can improve cognition and reduce neuroinflammation.
Ageing alters epithelial integrity, stem cell function, and autophagy capacity. We are investigating how these age-related shifts disrupt gut barrier function and accelerate systemic inflammation and neurovascular decline. This line of research intersects with menopause biology, neurovascular ageing, and chronic disease risk.
Meet the team
Group Leader
- Professor Erinna Lee
PhD researchers:
- Umairah Binte Abdul Khalid (2028)
- Olivia Stuart (2029)
Masters researchers:
- Yashodha Ralalage (2026)
Publications
See a full list of publications on: