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Cambridge Infectious Diseases

An Interdisciplinary Research Centre at the University of Cambridge


We study Pattern Recognition Receptors, such as Toll-like receptors (TLR), in different mammalian species studying their roles in responding to both purified bacterial ligands and infection with Salmonella entericia serovar Typhimurium (in collaboration with Duncan Maskell). We use gene arrays to study how bacterial gene expression changes in the phagosome of macrophages and use chimeric receptor constructs to study species-specific ligand interaction at the TLR4/MD2 complex (in collaboration with Nick Gay, Biochemistry). Currently we are studying the recruitment of adaptor proteins to TLR4, determining how S. Typhimurium bypasses the adaptor protein Mal during infection (in collaboration with Luke O’Neill, Dublin) and how S. Typhimurium activates the inflammasome. We work with Pietro Cicuta (Physics), Jochen Guck (Physics), Julia Gog (DAMPT) and Ray Goldstein (DAMPT) to study bacterial interactions with cells and respiratory tissues using mathematical modelling, optical tweezers, optical stretching and real-time imaging.


Our research focuses on using novel techniques to understand how innate immunity interfaces with host-pathogen interactions.  We use mathematical modeling to develop new questions about how the host interacts with bacteria and then develop the appropriate techniques to practically answer these questions.  We use classical structure-function analysis (transfection assays, macrophage studies, FRET and single molecule flourescence techniques) to study TLR-ligand interactions.  We study infection in vitro and in vivo.  In our in vitro studies we use traditional cell culture techniques, live cell confocal imaging, optical tweezers and optical stretching to explore how bacteria interact with cells and what the consequences of these interactions are for the host cell biology. 


Key publications: 

Bryant CE, Spring DR, Gangloff M, Gay NJ. (2010) “The molecular basis of the host response to lipopolysaccharide.” Nat Rev Microbiol. 8, 8-14

Wright, J.A., Tötemeyer, S., Hautefort, I., Appia-Ayme, C., Alston, M., Danino, V., Paterson, G.K., Mastroeni, P., Ménager, N., Rolfe, M., Thompson, A., Ugrinovic, S., Sait, L., Humprey, T., Northen, H., Peters, S.E., Maskell, D.J., Hinton, J.C.D. and Bryant, C.E. (2009) Multiple redundant stress resistance mechanisms are induced in Salmonella enterica serovar Typhimurium in response to alteration of the intracellular environment via TLR4 signalling.  Microbiology 155, 2919-29

Talbot, S., Tötemeyer, S., Yamamoto, M., Akira, S., Hughes, K., Gray, D., Barr, T., Mastroeni, P., Maskell, D.J. and Bryant, C.E. (2009) Toll-like receptor 4 signalling through MyD88 is essential to control Salmonella enterica serovar Typhimurium infection, but not for the initiation of bacterial clearance. Immunology 128, 472-83

Walsh, C.M., Gangloff, M., Monie, T., Smythe, T., Wei, B., McKinley, T.J., Maskell, D.J., Gay, N.J and Bryant, C.E.  (2008) Elucidation of the MD-2/TLR4 interface required for signalling by Lipid IVa.  J. Immunol. 181, 1245-54.

Núñez Miguel, R., Wong, J., Westoll, J.F., Brooks, H.J., O’Neill, L.A.J., Gay, N.J., Bryant, C.E. and Monie, T.P. (2007) A Dimer of the Toll-Like Receptor 4 Cytoplasmic Domain Provides a Specific Scaffold for the Recruitment of Signalling Adaptor Proteins.  PLoS One 2, e788

Royle, M.C.J., Tötemeyer, S., Maskell, D.J. and Bryant, C.E. (2003) Stimulation of TLR-4 by lipopolysaccharide during infection with live Salmonella typhimurium  is a critical, but not exclusive event leading to macrophage responses. J. Immunol. 170, 5445-5454

BBSRC Research Development Fellow
Professor Clare  Bryant
Takes PhD students
Available for consultancy


Departments and institutes: 
Person keywords: 
Innate Immunity