Professor Phil Sutton
Associate Professor Phil Sutton studied Biomedical Science at Bradford University in the UK before undertaking a PhD in Immunology at Manchester University. He moved to Australia in 1992 for his first postdoctoral position, and apart from a brief spell at Institut Pasteur de Lille in France, has been here ever since. Associate Professor Sutton has extensive experience in both academia and industry, including a period as Immunology group leader within the research and development division of CSL Limited, where he worked on vaccine development and adjuvant technologies.
Associate Professor Sutton is a National Health and Medical Research Council (NHMRC) Senior Research Fellow with continuous funding from the NHRMC, Australian Research Council and industry partners and is a scientific committee member of the European Study Group on Pathogenesis and Immunology in Helicobacter Infections. He moved the Mucosal Immunology group to Murdoch Childrens in 2012. The Mucosal Immunology group is focused on examining how the host regulates bacterial pathogenesis within the gastrointestinal tract, as well as research on mucosal vaccine development.
Bacterial-driven inflammation is a major cause of disease. This inflammation can arise as a result of infection by known pathogens such as Helicobacter pylori, the main causative agent of stomach and duodenal ulcers, and gastric cancer. Alternatively, inflammatory bowel disease is believed to result from inappropriate inflammatory reaction to normal gut flora.
The development of such diseases is highly complex, and not all individuals infected with a specific pathogen will develop a specific disease. Most people infected with H. pylori remain asymptomatic while those that develop symptoms can suffer a range of disease states. This complexity arises from the interaction of multiple factors, including differences in the bacterial pathogens themselves, as well as environmental factors that contribute to disease susceptibility, such as smoking or a high salt diet. Finally, genetic factors play significant roles in determining whether an individual is susceptible or resistant to disease development.
This last feature is a core focus of the group's research. The team is interested in host factors that contribute to susceptibility or resistance to diseases that result from bacterial-driven inflammation of the gastrointestinal (GI) tract. In this regard the team has several projects exploring the role that novel host factors play in regulating the severity of the inflammatory response mounted by a host to infection with a bacterial pathogen in the GI tract.
The group is also interested in strategies that allow the development of vaccines with improved effectiveness against mucosal pathogens. This has a particular emphasis on mucosal vaccine delivery.
- Vaccine development
- Infection and immunity in cystic fibrosis
- An immunotherapeutic for protecting against Helicobacter pylori associated diseases
- How mucins protect against bacterial-driven inflammation
Han J, Ng G, Cecchini P, Chionh Y, Saeed M, Naess L, Joachim M, Blandford L, Strugnell R, Colaco C & Sutton P. (2016) Heat shock protein complex vaccines induce antibodies against Neisseria meningitidis via a MyD88-independent mechanism. Vaccine 34: 1704-1711.
Ng G & Sutton P. (2016) The MUC1 mucin specifically inhibits activation of the NLRP3 inflammasome. Genes and Immunity 17: 203-206.
Ng G, Menheniott T, Every A, Stent A, Judd L, Chionh Y, Dhar P, Komen J, Giraud A, Wang T, McGuckin M & Sutton P. (2016) The MUC1 mucin protects against Helicobacter pylori pathogenesis in mice by regulation of the NLRP3 inflammasome. Gut 65: 1087-1099.
Ng G & Sutton P. (2015) An optimized perfusion technique for extracting murine gastric leukocytes. Journal of Immunological Methods 427: 126-129
Harbour S, Mitchell H & Sutton P. (2015) Host non-responsiveness does not interfere with vaccine-mediated protection against gastric Helicobacter infection. Helicobacter 20: 217-212.
Chionh Y, Ng G, Ong L, Arulmuruganar A, Stent A, M Saeed, Wee J & Sutton P. (2015) Protease Activated Receptor 1 suppresses Helicobacter pylori gastritis in mice via the inhibition of macrophage cytokine secretion and Interferon Regulatory Factor 5. Mucosal Immunology 8: 68-79.
Sutton P. (2015) At last, vaccine-induced protection against Helicobacter pylori. Lancet 386: 1424-1425
Timothy A, Tokanovic A, Snibson K, Edwards S, Pearse M, Scheerlinck J-P & Sutton P. (2015) ISCOMATRIX™ adjuvant reduces mucosal tolerance for effective pulmonary vaccination against influenza. Human Vaccines and Immunotherapeutics 11: 377-385.
Chionh Y, Arulmuruganar A, Venditti E, Ng G, Han J, Ang C, Entwisle C, Colaco C, McNulty S & Sutton P. (2014) Heat shock protein complex vaccination induces protection against Helicobacter pylori without exogenous adjuvant. Vaccine 32: 2350–2358
Stent A, Every A, Ng G, Chionh Y, Ong L, Edwards S & Sutton P. (2012) Helicobacter pylori thiolperoxidase as a protective antigen in single- and multi-component vaccines. Vaccine 30: 7214–7220
Sutton P. (2011) Vaccinating against Helicobacter pylori: dissecting the mechanism. Gastroenterology 141: 1149-1151
Every A, Ng G, Skene C, Harbour S, Walduck A, McGuckin M & Sutton P. (2011) Localized suppression of inflammation at sites of Helicobacter pylori colonisation. Infection and Immunity 79: 4186–4192
McGuckin M, Linden S, Sutton P & Florin T. (2011) Mucin Dynamics and Enteric Pathogens. Nature Reviews Microbiology 9: 265-278
Every A, Stent A, Moloney M, Ng G, Skene C, Edwards S & Sutton P. (2011) Evaluation of superoxide dismutase from Helicobacter pylori as a protective vaccine antigen. Vaccine 29: 1514-1518Vujanic A, Wee J, Snibson K, Edwards S, Pearse M, Quinn C, Moloney M, Taylor S, Scheerlinck J-P & Sutton P. (2010) Combined mucosal and systemic immunity following pulmonary delivery of ISCOMATRIX™ adjuvanted recombinant antigens. Vaccine 28: 2593-2597
Wee J, Chionh Y-T, Ng G, Harbour S, Allison C, Pagel C, Mackie E, Mitchell H, Ferrero R & Sutton P (2010) Protease Activated Receptor-1 down-regulates the murine inflammatory and humoral response to Helicobacter pylori . Gastroenterology 138: 573–582