Innate Immune Responses to Infection
Research Group Head
Director’s Research Group
The subversion of host cell processes by microbial pathogens is an intrinsic part of the host-pathogen interaction. Many bacterial pathogens have the ability to transport virulence proteins, called effector proteins, into host cells via specialised protein secretion systems. We work on a range of virulence effectors from pathogenic E. coli, Shigella and Salmonella that interfere with host innate immune signalling pathways and block inflammation and cell death. The aim of this work is to investigate the manipulation of host cell signalling by effector protein families to understand their influence on host cell function, inflammatory signalling and the innate immune response. In this way effector proteins can be used as tools to understand the innate responses important for control of the pathogen.
Many bacterial pathogens have acquired the capacity to replicate inside human cells by avoiding cell intrinsic innate immune pathways. Pathogens such as Legionella and Burkholderia are environmental organisms that cause the life threatening opportunistic infections known as Legionnaire’s Disease and Melioidosis respectively. A feature of both pathogens is the capacity of the bacteria to replicate within human cells through the manipulation of host cell biology. This depends on the ability of the pathogens to inject multiple virulence effector proteins into the host cell during infection. Our goal is to identify and characterise effectors that interact with cell intrinsic innate immune pathways. Ultimately this will allow us to understand the molecular mechanisms by which intracellular bacteria cause disease.
