The human gastrointestinal tract houses a large number of microbes, collectively known as the microbiota that supports host metabolism, immune development and pathogen resistance. Intestinal dysbiosis, disruption of bacterial diversity in the gut, can result from antibiotic use or pathogenic infection and has been strongly linked to increased disease susceptibility. This dysbiosis-induced susceptibility indicates that normal commensal bacteria are capable of preventing disease; however, mechanisms involved in key host-commensal interactions are still largely unknown.
We seek mechanistic insights into the influence of commensal microbes on both intestinal infections and inflammation and systemic immune responses. These fundamental insights will give us a better understanding of infectious diseases, autoimmune disorders and even cancer, and will enable the development of new approaches to combat these diseases. Using in vivo models, cellular immunology, transcriptomics and proteomics and working closely with the Wellcome Trust Sanger Institute, we characterise the complex interactions between the commensal microbial community, intestinal epithelium and adaptive immune cells.
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