Ker Memorial Prize 2014

Edinburgh Infectious Diseases was delighted to announce that the winner of the 2014 Ker Memorial Prize was Dr Chris Lucas in the Centre for Inflammation Research.

The Prize is awarded each year for the best PhD thesis submitted to the University of Edinburgh in infectious diseases.  It is made possible by the generous gift of Miss Aileen Ker (pronounced 'car') in memory of her father and grandfather, Drs Frank and Claude Ker, who were influential infectious diseases clinicians, practising in Edinburgh during the first half of the 20th century. 

This year we received five excellent nominations:

  • German Canton (Moredun Research Institute, Francesca Chianini and Frank Katzer's labs)
    • Immunopathogenesis of bovine Neosporosis throughout gestation
  • Chris Lucas (Centre for Inflammation Research, Adriano Rossi's lab)
    • Modulation of inflammatory cell apoptosis in infection–associated inflammation
  • Paul McAdam (Roslin Institute, Ross Fitzgerald's lab)
    • Population analysis of bacterial pathogens on distinct temporal and spatial scales
  • Chloe McIntyre (Roslin Institute, Peter Simmonds' lab)
    • The epidemiology, classification and evolution of human rhinoviruses
  • Lian Thomas (Institute of Immunology and Infection Research, Eric Fevre's lab)
    • Epidemiology of Taenia solium cysticercosis in western Kenya

The judges, Prof Mark Stevens (Roslin Institute) and Prof Gary Entrican (Moredun Research Institute) were extremely impressed with the quality and impact of all the nominees and it was hard task picking a winner.  However they decided that Chris's work on inflammatory cell apoptosis in infection–associated inflammation was outstanding and that he was a worthy winner of the Prize.  Click here to read a lay summary of Chris's thesis work.

Of Chris, Gary Entrican said

His research focused on functional aspects of neutrophils in relation to anti-bacterial immunity and associated inflammation. In particular, targeting an intracellular pathway that enhances neutrophil apoptosis and thereby reduces inflammation without compromising bacterial clearance. This is excellent science with great therapeutic potential which enhances the reputation of University of Edinburgh and Edinburgh Infectious Diseases.

Chris is a qualified clinician and carried out his PhD as part of the Edinburgh Clinical Academic Training (ECAT) programme.  Since completing his thesis he has returned to medicine and is currently a clinical lecturer in respiratory medicine focusing on understanding and manipulating resolution of inflammation pathways in both sterile and infection-associated acute inflammation. 

As part of the prize Chris received £500, and presented his thesis work at the  Edinburgh Infectious Diseases symposium on Wednesday 21 May at the Royal College of Physicians. 

Many congratulations!


Lay summary of Chris's thesis work

Inflammation, the response of tissues to injury, is usually a beneficial response aimed at protecting humans from invading pathogens and tissue injury. However, it is vitally important that the inflammatory response is controlled to prevent ongoing tissue injury. Indeed, unresolved inflammation underpins multiple human diseases including acute lung infection (pneumonia) and sepsis.

Pneumonia is a common and serious condition affecting developed and developing countries. Despite advances in intensive care treatment and antimicrobial therapy mortality from pneumonia has not fallen since the 1950s. In over half of patients with pneumonia no causative organism is ever isolated which suggests that although the immune response has successfully controlled infection continued uncontrolled inflammation in the lung continues to cause morbidity and mortality. Understanding the mechanism behind such uncontrolled, persisting inflammation is therefore both urgent and essential, as is the need for novel approaches to target infection-related lung injury.

The resolution of inflammation was traditionally regarded as a passive process, secondary to decreases in pro-inflammatory mediators. However, it has been demonstrated that spontaneous resolution of inflammation is a tightly controlled energy-dependent process, key to which are the processes of neutrophil cell death (by apoptosis) and subsequent engulfment by surrounding cells including macrophages. Manipulation of these powerful processes governing the spontaneous resolution of inflammation may therefore be exploited for therapeutic gain and represent novel pharmacological targets for anti-inflammatory therapies.

We therefore examined the potential of neutrophil apoptosis-inducing drugs as potential treatments for infection-associated lung inflammation and the consequences on bacterial clearance. The primary agents used included a cyclin-dependent kinase inhibitor (an anti-cancer drug) as well as a plant-derived product (a flavone). These compounds induced human neutrophil apoptosis in vitro, and accelerated resolution in models of inflammation. This potential therapeutic approach was also found to have indirect anti-bacterial effects in a model of bacterial (E. Coli) pneumonia, in stark contrast to established anti-inflammatory approaches that routinely predispose towards life threatening infection. As such, targeting inflammatory cell apoptosis offers a potential new therapeutic approach for the treatment of infection-associated inflammation.


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