Dr Helen Marriott PhD
Department of Infection and Immunity
K Floor, (Office K105)
The University of Sheffield Medical School
Beech Hill Road
Tel: +44 (0)114 271 2181
Fax: +44 (0)114 226 8898
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.
My main research interest is in the role of macrophages in host defense against respiratory pathogens, in particular Streptococcus pneumoniae. Additionally, I am 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 Dr Colin Bingle. My work on the development of computational models is in collaboration with Dr Alex Best (Mathematics and Statistics), Professor Rod Smallwood (Computer Science) and Professor Mike Boots (University of Exeter).
My main teaching interest is in supporting the development of strong fundamental research skills in students. I contribute to several modules in the MSc in Molecular Medicine, I am module leader for the Experimental Medicine pathway modules 'Molecular and Cellular Basis of Disease' and 'Model Systems in Medical Research', and the Microbes and Infection pathway module 'Pathogenicity of Viruses and Fungi'. I also teach on the Postgraduate Induction course of the Faculty of Medicine, Dentistry and Health.
- Committee member of the British Association for Lung Research.
- Member of University of Sheffield ethical review panel/3Rs Committee.
- Computational models of macrophage innate immune responses to Staphylococcus aureus.
- Role of ubiquitination in regulation of macrophage viability after bacterial infection.
- The role of apoptosis in murine models of pneumococcal pneumonia.
- H.M. Marriott, M. Daigneault, A.A.R. Thompson, S.R. Walmsley S. Gill, D.R. Witcher V. Wroblewski, P.G. Hellewell, MKB Whyte and DH Dockrell. A Decoy Receptor 3 Analogue Reduces Localized Defects in Phagocyte Function in Pneumococcal Pneumonia. Thorax 2012 67(11):895-92.
- H.M. Marriott, K.A. Gascoyne, R. Gowda, I. Geary, M.J.H. Nicklin, F. Iannelli, G. Pozzi, T.J. Mitchell, M.K.B. Whyte, I. Sabroe, and D.H. Dockrell. IL-1β regulates CXCL8 release and influences disease outcome in response to Streptococcus pneumoniae, defining intercellular cooperation between pulmonary epithelial cells and macrophages. Infection and Immunity 2012 Mar;80(3):1140-9.
- M. Daigneault, J.A. Preston, H.M. Marriott, M.K. Whyte and D.H. Dockrell. The identification of markers of macrophage differentiation in PMA-stimulated THP-1 cells and monocyte-derived macrophages. PLoS One 2010: 5:e8668.
- 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.