Lister Fellow Sophie Helaine Publishes in Science

We are pleased to announce that one of our 2017 Lister Institute Research Prize winners Dr. Sophie Helaine has recently published a new research paper in the prestigious journal Science. The paper explains Dr. Helaine’s (and her collaborators’) research into bacterial ‘persister cells’ and may have significant implications for some aspects of future therapies and research in this important area of medicine.

Persister cells are bacteria that possess the ability to trigger repeated infections in some people by assuming a dormant state upon entering the body, and re-activating at a later date. The new paper discusses research into how persister cells can manipulate immune cells in the body and could potentially indicate new approaches to how persister cells can be killed; reducing or preventing recurring bacterial infections.

The new findings might also help researchers and clinicians understand why some people are more susceptible to recurrences of particular illnesses, despite undergoing treatment with antibiotics.

Persister cells were discovered in 1944 and for the case of Salmonella are found within macrophages in the human body. Macrophages play an important role in the body’s immune defence processes; engulfing and degrading viruses and bacteria that would otherwise cause harm and protecting us from their effects.

Dr. Helaine and her colleagues have found that not only are persister cells ‘hiding’ in macrophages and re-activating at a later date, they can also damage the macrophage’s abilities to fight the infection in doing so.

This important finding raises serious concerns relating to bacterial infections. It was previously thought that persister cells were essentially inactive while in their dormant state within the macrophage. Dr. Helaine’s team have identified that they actually play a role in weakening the macrophage while in this state, leading to a potentially significant reduction in the body’s immunity-based defence system.

The research primarily focussed on the Salmonella bacteria, as they are very common and make a highly suitable subject sample to study. In order to assess the propensity of the bacterium to affect the macrophage, the team infected macrophages derived from mouse bone marrow with Salmonella cells carrying a ‘reporter plasmid’ to enable tracking of bacterial proliferation and activity.

As Dr. Helaine explains:

This work on how Salmonella persisters manipulate the host innate immune defense cells is the result of a fruitful collaboration with the Vogel lab in Germany and was carried out brilliantly in my lab by two very talented postdoctoral researchers, Dr Daphne Stapels and Dr Peter Hill. Daphne came as an EMBO fellow in the lab but when her fellowship ran out, the support from the Lister Institute became instrumental for us to complete the work. I am extremely grateful to the Lister Institute for their invaluable support and their recognition of our research.”

The paper is entitled Salmonella persisters undermine host immune defenses during antibiotic treatment and was published in Vol 362, Issue 6419 of Science by the American Association for the Advancement of Science. The research on which the paper was based also involved scientists working with the Vogel lab at the Helmholtz Institute for RNA-based Infection Research in Germany.

Dr. Helaine is a Senior Lecturer in the Faculty of Medicine at Imperial College London. She is affiliated with the Centre for Molecular Bacteriology and Infection (CMBI) based at the university, and her work was also funded by an MRC Career Development Award for her research into how persisters interact with their host.

Dr. Helaine completed a PhD at Campus Necker – Paris V, Universite Paris in 2006 with Dr. Vladimir Pelicic before joining the CMBI as a Research Associate in the laboratory of Professor David Holden.

We are very pleased to have played a role in supporting Dr. Helaine’s work through her award of a Lister Institute Research prize, and are looking forward to hearing more about her success in the future.