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Host-pathogen interactions,Bacterial pathogenesis,Bacterial intestinal infections,Inflammatory bowel disease,Legionnaire's disease
Many bacterial pathogens have acquired the capacity to attach to and/or replicate inside human cells by avoiding cell intrinsic innate immune pathways. The subversion of host cell signaling by pathogens frequently depends on the ability to transport virulence proteins, called effector proteins, into the infected cell via specialised protein secretion systems. We work on a range of virulence effectors from pathogenic bacteria that interfere with host innate immune signalling pathways and block inflammation and cell death. In this way effector proteins can be used as tools to understand the innate responses important for control of the pathogen. Our long term goal is to uncover new host processes and structures that are targeted by bacteria during infection leading to the design and development of novel anti-infective agents to treat a range of infectious diseases.
Genetic manipulation of bacterial pathogens
In vivo models of infection
Protein-protein interactions
Host-pathogen imaging
Innate immune signalling
Effector protein biochemistry
John Silke# WEHI,Andreas Strasser# WEHI,Gad Frankel# Imperial College London,Professor Ian van Driel# University of Melbourne,Professor Carmen Buchrieser# Institute Pasteur
Mouse model of Legionnaire's disease
Mouse models of gastrointestinal infection
- Targeting of microvillus protein Eps8 by the NleH effector kinases from enteropathogenic E. coli.
- Inhibition of the master regulator of Listeria monocytogenes virulence enables bacterial clearance from spacious replication vacuoles in infected macrophages.
- Structural and Functional Characterization of Legionella pneumophila Effector MavL.
- Genome-wide genetic screen identifies host ubiquitination as important for Legionella pneumophila Dot/Icm effector translocation.
- Emerging methods in cellular microbiology.
- NleB2 from enteropathogenic Escherichia coli is a novel arginine-glucose transferase effector.
- Effectors Targeting the Unfolded Protein Response during Intracellular Bacterial Infection.
- IFNγ receptor down-regulation facilitates Legionella survival in alveolar macrophages.
- Loss of O-Linked Protein Glycosylation in Burkholderia cenocepacia Impairs Biofilm Formation and Siderophore Activity and Alters Transcriptional Regulators.
- Salmonella Effectors SseK1 and SseK3 Target Death Domain Proteins in the TNF and TRAIL Signaling Pathways.
- Targeting of RNA Polymerase II by a nuclear Legionella pneumophila Dot/Icm effector SnpL.
- The bacterial arginine glycosyltransferase effector NleB preferentially modifies Fas-associated death domain protein (FADD).
- Identification of a Distinct Substrate-binding Domain in the Bacterial Cysteine Methyltransferase Effectors NleE and OspZ.
