NEC, gut "omics" and enteroids
The key focus of our research group is to better understand the factors leading to the development of necrotising enterocolitis (NEC). This is important because more babies die from NEC than all cases of childhood leukemia, yet the mechanisms leading to disease are poorly understood.
Applying high-throughput next generation sequencing and mass spectrometry-based approaches to generate comprehensive data from clinical samples, such as stool, nasopharyngeal aspirate, saliva, oral swabs, tissue resections, and blood. Such datasets typically include information relating to the presence of microbes and their genetic capacity, as well as microbial and host protein and metabolite levels.
Bioinformatics and statistical analysis can then be applied to determine differences between diseased and control groups, plus what specific microbes/genes/proteins/metabolites are associated with each group. Although disease mechanism requires further work, this area of discovery research typically yields several testable hypotheses. You can read more about our research here.
Due to recent scientific advances, we now have the ability to take patient tissue that would otherwise be discarded and derive intestinal ‘enteroids’ from the tissue. These human intestinal enteroids are able to grow into ‘mini guts’ in the laboratory and can differentiate into all the major cell types of the intestine. They also secrete mucin and respond to viral or bacterial infection.
Because the tissue is derived from patients with disease, and retains the genetic, epigenetic, and exposure history, human intestinal enteroids have several major advances over animal models. With collaborators at Baylor College of Medicine (Houston, USA), we have pioneered a powerful co-culture system that mimics the conditions of the gastrointestinal tract and simultaneously allows bacteria and patient-derived enteroids to interact directly. We can then test how the addition of specific bacteria influences the health or disease status of the cells, such as by measuring epithelial integrity, bacterial translocation, and markers of disease (e.g., inflammatory cytokines). This work allows microbial-host cross-talk to be investigated and can lead to mechanistic understanding of disease processes, which can be directly translated into the clinical care of patients
The key focus of our research group is to better understand the factors leading to the development of necrotising enterocolitis (NEC). This is important because more babies die from NEC than all cases of childhood leukemia, yet the mechanisms leading to disease are poorly understood.
Applying high-throughput next generation sequencing and mass spectrometry-based approaches to generate comprehensive data from clinical samples, such as stool, nasopharyngeal aspirate, saliva, oral swabs, tissue resections, and blood. Such datasets typically include information relating to the presence of microbes and their genetic capacity, as well as microbial and host protein and metabolite levels.
Bioinformatics and statistical analysis can then be applied to determine differences between diseased and control groups, plus what specific microbes/genes/proteins/metabolites are associated with each group. Although disease mechanism requires further work, this area of discovery research typically yields several testable hypotheses. You can read more about our research here.
Due to recent scientific advances, we now have the ability to take patient tissue that would otherwise be discarded and derive intestinal ‘enteroids’ from the tissue. These human intestinal enteroids are able to grow into ‘mini guts’ in the laboratory and can differentiate into all the major cell types of the intestine. They also secrete mucin and respond to viral or bacterial infection.
Because the tissue is derived from patients with disease, and retains the genetic, epigenetic, and exposure history, human intestinal enteroids have several major advances over animal models. With collaborators at Baylor College of Medicine (Houston, USA), we have pioneered a powerful co-culture system that mimics the conditions of the gastrointestinal tract and simultaneously allows bacteria and patient-derived enteroids to interact directly. We can then test how the addition of specific bacteria influences the health or disease status of the cells, such as by measuring epithelial integrity, bacterial translocation, and markers of disease (e.g., inflammatory cytokines). This work allows microbial-host cross-talk to be investigated and can lead to mechanistic understanding of disease processes, which can be directly translated into the clinical care of patients