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Research in the Thurston laboratory seeks to understand what determines the fate of intracellular bacteria, a complex interaction mediated by both the host and the pathogen. On the host side, our research focuses on cell-intrinsic innate immune mechanisms that protect against intracellular bacteria. To complement this, our other area of research focuses on how Salmonella effector proteins, delivered into host cells, manipulate innate immune signaling.
Research in the Thurston laboratory is funded by the BBSRC as well as an MRC research grant awarded in 2021 and an ERC Starting Grant due to start in 2022. In addition, from 2022 we are an official Crick Satellite group at the Francis Crick Institute where we work closely with our collaborator Dr. Katrin Rittinger.
Teresa completed her PhD in 2010 with Dr. Felix Randow, at the Laboratory of Molecular Biology, University of Cambridge. During this time and a short postdoc period, she worked on understanding how antibacterial autophagy functions as a cell autonomous innate immune mechanism to restrict the growth of cytosolic bacteria.
In 2011, Teresa joined the CMBI as a postdoc in the laboratory of Prof. David Holden, focusing on Salmonella as a model intracellular pathogen. She was awarded an Early Career Research Fellowship from the Leverhulme Trust in 2012 and an Imperial College Research Fellowship in 2014 to establish her own research focused on innate immune signaling during Salmonella infection.
In July 2018 Teresa took up a 5 year BBSRC David Phillips Fellowship within the CMBI to continue investigating host-pathogen interactions. The goal of this research is to use a multidisciplinary approach encompassing proteomics, genetic screens, cell biology and structural biology, to identify and investigate how both host and pathogen determinants alter the outcome of bacterial infections. Such fundamental research into understanding host-pathogen interactions is needed to provide valuable insight into the pathophysiology of bacterial infections and represents an essential step for future research into novel therapeutic strategies.
Panagi I, Thurston TL, 2023, Ready, STAT3, Go! Bacteria in the race for M2 macrophage polarisation., Curr Opin Microbiol, Vol:73
et al., 2022, Pneumolysin suppresses the initial macrophage pro-inflammatory response to Streptococcus pneumoniae, Immunology, Vol:167, ISSN:0019-2805, Pages:413-427
et al., 2022, A role for the RNA polymerase gene specificity factor sigma(54) in the uniform colony growth of uropathogenic escherichia coli, Journal of Bacteriology, Vol:204, ISSN:0021-9193, Pages:1-16
Schroeder GN, Pearson JS, Thurston TLM, 2021, Editorial: bacterial effectors as drivers of human disease: models, methods, mechanisms., Frontiers in Cellular and Infection Microbiology, Vol:11, ISSN:2235-2988, Pages:1-4
et al., 2021, TIRAP in the mechanism of inflammation, Frontiers in Immunology, Vol:12, ISSN:1664-3224, Pages:1-12