Dealing with differential immune challenge: prokaryote / eukaryote co-infections
Applicants (UK, EU and international) capable of self-funding or with scholarship are welcome to apply.
Primary Supervisor: Dr Joanne Lello
Secondary Supervisors: Dr Jo Cable & Prof John Harwood
External Supervisor: Dr Sheena Cotter (Queen’s University, Belfast)
The immune defence against prokaryotic and eukaryotic organisms is differentiated, with greater defence levelled against prokaryotes. Two hypotheses can be proposed to explain this difference: i) that the stronger anti-prokaryote response is “hardwired” due to the longer evolutionary relationship between prokaryote pathogens and hosts or; ii) that hosts adaptively respond to the most pathogenic organism and that it is simply co-incidental that relatively few eukaryotes are highly pathogenic. In natural systems, prokaryote with eukaryote co-infections regularly occur. During this PhD, the student will examine the levels of anti-prokaryote/eukaryote immune responses to determine whether the immune system can respond adaptively to the most pathogenic organism or whether the anti-prokaryote response is always the “winning” effect. They will also determine whether host resource availability affects this process. To do this, they will infect a model host species (the German cockroach), with single or mixed combinations, of four different pathogens: 1) an endemic eukaryote protozoan with low level pathogenicity; 2) an axenic (i.e. without its symbiotic bacteria) entomopathogenic nematode, which while being a eukaryotic shows high pathogenicity, 3) the Xenhorabdus bacterial symbiont of the nematode, which is a prokaryotic and highly pathogenic organism, and 4) a low pathogenicity commensal bacterial species. Hosts will be provisioned at high, normal and low levels and immune responses will be monitored with standardised assays including encapsulation, lysozyme, antimicrobial peptides and phenoloxidase. Within host resource availability and provisioning to the immune system will be assessed via lipid analysis including assessment of potential lipid signalling molecules. This work will add to our fundamental understanding of host-pathogen interactions which will ultimately aid the development of pathogen control strategies.