Dr Helen Marriott PhD
Department of Infection and Immunity
L Floor
The University of Sheffield Medical School
Beech Hill Road
Sheffield
S10 2RX
United Kingdom
Tel: +44 (0)114 271 2439
Fax: +44 (0)114 226 8898
Email: h.m.marriott@sheffield.ac.uk
Biography
I joined the University of Sheffield in 1995 from the Department of Respiratory Physiology, Papworth Hospital, Cambridge. From 1995 to 2001 my research was on the pulmonary circulation, focusing on animal models of pulmonary hypertension. This formed the basis of my PhD, "Pulmonary hypertension: susceptibility and treatment in rat models".
In 2001 I joined Professor David Dockrell´s group as a post-doctoral research associate investigating the role of macrophage apoptosis in pneumococcal infection. In 2005 I was awarded an independent fellowship from the British Lung Foundation to investigate the effects of influenza A virus on macrophage innate immune function.
I am currently funded by a Research Council UK discipline hopping award to develop computational models of innate immune response to respiratory pathogens, based in Computational Systems Biology in the Department of Computer Science, Faculty of Engineering, University of Sheffield.
Research Interests
My main research interest is in the role of macrophages in host defense against respiratory pathogens. I am particularly interested in the effect of influenza A virus on macrophage function, its effect on the regulation of macrophage apoptosis and how this may lead to increased susceptibility to bacterial superinfections. I have been using a variety of in vitro and in vivo models and am currently developing computational models to support this research.
My main collaboration is with Professor David Dockrell. I also collaborate on murine in vivo models with Professor Moira Whyte, Dr Sarah Walmsley and Profesor Robert Read. My work on the development of computational models is in collaboration with Professor Rod Smallwood (Computer Science) and Professor Mike Boots (APS).
Teaching Interests
My main teaching interest is in supporting the development of strong fundamental research skills in students. I lead a practical training module in the MSc in Molecular Medicine and also contribute to several modules in the MSc in Molecular Medicine.
Professional Activities
- Committee member of the British Association for Lung Research.
- Member of University of Sheffield ethical review panel/3Rs Sub-Committee.
Current Projects
- Computational models of innate immune response to respiratory pathogens.
- Maintenance of macrophage viability after Neisseria meningitidis infection.
- The role of apoptosis in murine models of pneumococcal pneumonia.
Key Publications
- H.M. Marriott, L.E. Jackson P.G. Hellewell, M.K.B. Whyte and D.H. Dockrell. NADPH oxidase deficiency improves outcome in a murine model of pneumococcal pneumonia. American Journal Respiratory and Critical Care Medicine, 2008; 177:887-895.
- H.M. Marriott, P.G. Hellewell, M.K.B. Whyte and D.H. Dockrell. Contrasting roles for reactive oxygen species and nitric oxide in the innate response to pulmonary infection with Streptococcus pneumoniae. Vaccine, 2007; 22;25(13):2485-90.
- H.M. Marriott, P.G. Hellewell, S.S. Cross, P.G. Ince, M.K.B. Whyte and D.H. Dockrell. Decreased alveolar macrophage apoptosis is associated with increased pulmonary inflammation in a murine model of pneumococcal pneumonia. The Journal of Immunology, 2006; 177: 6480-6488.
- H.M. Marriott, C.D. Bingle, R.C. Read, K.E. Braley, R.W. Craig, G. Kroemer, P.G. Hellewell, M.K.B. Whyte and D.H. Dockrell. Dynamic Changes in Mcl-1 Expression Regulate Macrophage Viability or Commitment to Apoptosis during Bacterial Clearance. Journal of Clinical Investigation, 2005; 115:359-368.
- H.M. Marriott, F. Ali, R.C. Read, T.J. Mitchell, M.K.B. Whyte and D.H. Dockrell. iNOS-dependent NO production by differentiated human macrophages induces microbial killing and macrophage apoptosis. FASEB J, 2004; 18(10):1126-8.
- D.H. Dockrell, H.M. Marriott, L.R. Prince, V.C. Ridger, P.G. Ince, P.G. Hellewell and M.K.B. Whyte. Alveolar macrophage apoptosis contributes to pneumococcal clearance in a resolving model of pulmonary infection. The Journal of Immunology, 2003; 171: 5380–5388.
