Dr Phil Elks

Sir Henry Dale Fellow

Department of Infection, Immunity & Cardiovascular DiseasePhil Elks
D31a, Firth Court
Western Bank
Sheffield S10 2TN
United Kingdom

Tel: +44 (0) 114 222 3609
Fax: +44 (0) 114 226 8898
Email:  p.elks@sheffield.ac.uk

Secretary: Mrs Susan Clary
Tel: +44 (0) 114 215 9503
Email: s.clary@sheffield.ac.uk


I graduated with a BSc (hons) in Biochemistry at the University of Warwick in 2004. I moved to Sheffield for the first time in 2004 to pursue a PhD in bone biology in a collaborative project between the, then newly forming, Centre for Developmental and Biomedical Genetics (CDBG) (with Dr Henry Roehl) and the Medical School (with Professor Peter Croucher), in which I studied the role of Wnt signalling in osteoblast formation in zebrafish. After my PhD I did a post-doctoral project with Dr Stephen Renshaw, in which I investigated hypoxia-induced genetic signalling (HIF signalling) and its role in inflammation. During this project I developed the zebrafish as a model to study HIF signalling, and I was awarded a European Respiratory Society (ERS) Long Term Fellowship in 2011 to study HIF’s role in infection. I moved to the University of Leiden, The Netherlands, to perform the ERS Fellowship, in which I found a role for HIF in the host-defence mechanism against Tuberculosis in a zebrafish model. In 2013 I was awarded a Vice-Chancellor’s Fellowship to return to Sheffield and set up my research group in Infection and Immunity.  In 2015 I was awarded a Sir Henry Dale Fellowship from The Wellcome Trust/Royal Society.

Research Interests:

When the body encounters invading pathogens, such as bacteria, a series of interactions between host immune cells and pathogen is initiated. These interactions are highly dynamic and involve complex genetic signalling pathways deriving from both the host and the pathogen. White blood cells, or leukocytes, of the host are able to phagocytose (internalise) bacteria and have an artillery of killing mechanisms to disarm the infection. However some bacteria, such as Mycobacterium tuberculosis, have evolved to survive and proliferate within host immune cells, disarming the leukocytes to make a niche in which to prosper. These types of infection have been historically successfully treated by targeting the bacteria using antibiotics. However, more recently, there has been an alarming rise in strains which are multi-drug resistant. Further understanding of the host response to infection is required to identify genetic targets for much needed future host-targetted therapies.

One host-genetic pathway that I have previously identified as being a modulator of both inflammation and infection is the HIF pathway, an important cellular oxygen sensing pathway. In the normal oxygen situation the HIF transcription factor is silenced by protein degradation, however during inflammatory and infection situations HIF is stabilised in leukocytes, via mechanisms that have yet to be fully elucidated, and has a number of immune activating effects. HIF therefore represents a potential host-derived target for therapeutics against infectious disease.

The zebrafish is my chosen model to study the roles of HIF in host response to infection. The zebrafish embryo is transparent and genetically manipulable, allowing a unique opportunity in which to study the host response to infection in a whole organism setting. Utilizing zebrafish models of infection I hope to shed light on the roles of HIF during infection, and to further understand the complex signalling processes involved in host-pathogen interaction.

Professional Activities:

  • Vice-Chancellor’s Fellow.
  • Member of the European Respiratory Society.
  • Reviewer of manuscripts.
  • Supervisor of students (BMedSci/ bachelors/ masters). 


For Key Publications see below.  For a full list of publications click here.

Journal articles

Conference proceedings papers